Publications

@article{pmid38754802,

title = {Uninterrupted in vivo cerebral microdialysis measures of the acute neurochemical response to a single or repeated concussion in a rat model combining force and rotation},

author = {Ian Massé and Luc Moquin and Caroline Bouchard and Alain Gratton and Louis De Beaumont},

doi = {10.1016/j.brainres.2024.148998},

issn = {1872-6240},

year  = {2024},

date = {2024-09-01},

journal = {Brain Res},

volume = {1838},

pages = {148998},

abstract = {Altered extracellular amino acid concentrations following concussion or mild traumatic brain injury can result in delayed neuronal damage through overactivation of NMDA glutamatergic receptors. However, the consequences of repeated concussions prior to complete recovery are not well understood. In this study, we utilized in vivo cerebral microdialysis and a weight-drop model to investigate the acute neurochemical response to single and repeated concussions in adult rats that were fully conscious. A microdialysis probe was inserted into the hippocampus and remained in place during impact. Primary outcomes included concentrations of glutamate, GABA, taurine, glycine, glutamine, and serine, while secondary outcomes were righting times and excitotoxic indices. Compared to sham injury, the first concussion resulted in significant increases in glutamate, GABA, taurine, and glycine levels, longer righting times, and higher excitotoxic indices. Following the second concussion, righting times were significantly longer, suggesting cumulative effects of repeated concussion while only partial increases were observed in glutamate and taurine levels. GABA and glycine levels, and excitotoxic indices were comparable to sham injury. These findings suggest that single and repeated concussions may induce acute increases in several amino acids, while repeated concussions could exacerbate neurological symptoms despite less pronounced neurochemical changes.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38733756,

title = {Hair steroid before and after COVID-19 in preschoolers: the moderation of family characteristics},

author = {Éloise Berger and Marie-Pier Larose and France Capuano and Marie-Josée Letarte and Marie-Claude Geoffroy and Sonia Lupien and Mara Brendgen and Michel Boivin and Frank Vitaro and Richard Tremblay and Benoît Masse and Sylvana Côté and Isabelle Ouellet-Morin},

doi = {10.1016/j.psyneuen.2024.107072},

issn = {1873-3360},

year  = {2024},

date = {2024-08-01},

journal = {Psychoneuroendocrinology},

volume = {166},

pages = {107072},

abstract = {BACKGROUND: Frequent or prolonged exposure to stressors may jeopardize young children's health. The onset of the COVID-19 pandemic, coupled with disruptions in daily routines and social isolation resulting from public health preventive measures, have raised concerns about its potential impact on children' experienced stress, particularly for young children and vulnerable families. However, whether the pandemic was accompanied by changes in physiological stress remains unknown as perceived stress is not a good proxy of physiological stress. This study examined if preschoolers showed increasing hair steroid concentrations following the onset of the COVID-19 pandemic and whether family characteristics may have exacerbated or buffered these changes.nnMETHODS: 136 preschoolers (2-4 years) provided hair for steroid measurement (cortisol, dehydroepiandrosterone (DHEA), cortisone, cortisol-to-DHEA ratio, cortisol-to-cortisone ratio) in October-November 2019 (T0) and in July-August 2020 (T1). A 2-centimeter hair segment was analyzed, reflecting steroid production over the two months leading up to collection. Family income, conflict resolution and lack of cohesion, as well as parents' COVID-19 stress were reported by parents. Linear mixed models for repeated measures and Bayes factors were used.nnRESULTS: No significant changes were noted from before to after the onset of the COVID-19 pandemic for most hair steroids. However, a moderating role of family conflict resolution was noted. Children living with parents with a better ability to resolve conflicts had lower levels of DHEA compared to those who had more difficulty managing conflicts. Additionally, lower levels of family cohesion and income were linked to some steroids, especially DHEA, suggesting that these factors may relate to children's physiological stress. Finally, boys had higher DHEA levels than girls.nnCONCLUSION: Our findings suggest that stress biomarkers were comparable from before to during the COVID-19 pandemic. This observation holds true despite the pandemic being perceived by many as a novel, unpredictable, and potentially threatening event. Findings further suggest that family characteristics are associated with hair steroid, especially DHEA, which deserves further investigation.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38796098,

title = {The influence of circadian rhythms on CD8 T cell activation upon vaccination: A mathematical modeling perspective},

author = {Nasri Balit and Nicolas Cermakian and Anmar Khadra},

doi = {10.1016/j.jtbi.2024.111852},

issn = {1095-8541},

year  = {2024},

date = {2024-08-01},

journal = {J Theor Biol},

volume = {590},

pages = {111852},

abstract = {Circadian rhythms have been implicated in the modulation of many physiological processes, including those associated with the immune system. For example, these rhythms influence CD8 T cell responses within the adaptive immune system. The mechanism underlying this immune-circadian interaction, however, remains unclear, particularly in the context of vaccination. Here, we devise a molecularly-explicit gene regulatory network model of early signaling in the naïve CD8 T cell activation pathway, comprised of three axes (or subsystems) labeled ZAP70, LAT and CD28, to elucidate the molecular details of this immune-circadian mechanism and its relation to vaccination. This is done by coupling the model to a periodic forcing function to identify the molecular players targeted by circadian rhythms, and analyzing how these rhythms subsequently affect CD8 T cell activation under differing levels of T cell receptor (TCR) phosphorylation, which we designate as vaccine load. By performing both bifurcation and parameter sensitivity analyses on the model at the single cell and ensemble levels, we find that applying periodic forcing on molecular targets within the ZAP70 axis is sufficient to create a day-night discrepancy in CD8 T cell activation in a manner that is dependent on the bistable switch inherent in CD8 T cell early signaling. We also demonstrate that the resulting CD8 T cell activation is dependent on the strength of the periodic coupling as well as on the level of TCR phosphorylation. Our results show that this day-night discrepancy is not transmitted to certain downstream molecules within the LAT subsystem, such as mTORC1, suggesting a secondary, independent circadian regulation on that protein complex. We also corroborate experimental results by showing that the circadian regulation of CD8 T cell primarily acts at a baseline, pre-vaccination state, playing a facilitating role in priming CD8 T cells to vaccine inputs according to the time of day. By applying an ensemble level analysis using bifurcation theory and by including several hypothesized molecular targets of this circadian rhythm, we further demonstrate an increased variability between CD8 T cells (due to heterogeneity) induced by its circadian regulation, which may allow an ensemble of CD8 T cells to activate at a lower vaccine load, improving its sensitivity. This modeling study thus provides insights into the immune targets of the circadian clock, and proposes an interaction between vaccine load and the influence of circadian rhythms on CD8 T cell activation.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38670238,

title = {Microglial function interacts with the environment to affect sex-specific depression risk},

author = {Eamon Fitzgerald and Irina Pokhvisneva and Sachin Patel and Shi Yu Chan and Ai Peng Tan and Helen Chen and Patricia Pelufo Silveira and Michael J Meaney},

doi = {10.1016/j.bbi.2024.04.030},

issn = {1090-2139},

year  = {2024},

date = {2024-07-01},

journal = {Brain Behav Immun},

volume = {119},

pages = {597--606},

abstract = {There is a two-fold higher incidence of depression in females compared to men with recent studies suggesting a role for microglia in conferring this sex-dependent depression risk. In this study we investigated the nature of this relation. Using GWAS enrichment, gene-set enrichment analysis and Mendelian randomization, we found minimal evidence for a direct relation between genes functionally related to microglia and sex-dependent genetic risk for depression. We then used expression quantitative trait loci and single nucleus RNA-sequencing resources to generate polygenic scores (PGS) representative of individual variation in microglial function in the adult (UK Biobank; N = 54753-72682) and fetal (ALSPAC; N = 1452) periods. The adult microglial PGS moderated the association between BMI (UK Biobank; beta = 0.001, 95 %CI 0.0009 to 0.003, P = 7.74E-6) and financial insecurity (UK Biobank; beta = 0.001, 95 %CI 0.005 to 0.015, P = 2E-4) with depressive symptoms in females. The fetal microglia PGS moderated the association between maternal prenatal depressive symptoms and offspring depressive symptoms at 24 years in females (ALSPAC; beta = 0.04, 95 %CI 0.004 to 0.07, P = 0.03). We found no evidence for an interaction between the microglial PGS and depression risk factors in males. Our results illustrate a role for microglial function in the conferral of sex-dependent depression risk following exposure to a depression risk factor.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38677627,

title = {Examining the associations between microglia genetic capacity, early life exposures and white matter development at the level of the individual},

author = {Shi Yu Chan and Eamon Fitzgerald and Zhen Ming Ngoh and Janice Lee and Jasmine Chuah and Joanne S M Chia and Marielle V Fortier and Elizabeth H Tham and Juan H Zhou and Patricia P Silveira and Michael J Meaney and Ai Peng Tan},

doi = {10.1016/j.bbi.2024.04.038},

issn = {1090-2139},

year  = {2024},

date = {2024-07-01},

journal = {Brain Behav Immun},

volume = {119},

pages = {781--791},

abstract = {There are inter-individual differences in susceptibility to the influence of early life experiences for which the underlying neurobiological mechanisms are poorly understood. Microglia play a role in environmental surveillance and may influence individual susceptibility to environmental factors. As an index of neurodevelopment, we estimated individual slopes of mean white matter fractional anisotropy (WM-FA) across three time-points (age 4.5, 6.0, and 7.5 years) for 351 participants. Individual variation in microglia reactivity was derived from an expression-based polygenic score(ePGS) comprised of Single Nucleotide Polymorphisms (SNPs) functionally related to the expression of microglia-enriched genes.A higher ePGS denotes an increased genetic capacity for the expression of microglia-related genes, and thus may confer a greater capacity to respond to the early environment and to influence brain development. We hypothesized that this ePGS would associate with the WM-FA index of neurodevelopment and moderate the influence of early environmental factors.Our findings show sex dependency, where a significant association between WM-FA and microglia ePGS was only obtained for females.We then examined associations with perinatal factors known to decrease (optimal birth outcomes and familial conditions) or increase (systemic inflammation) the risk for later mental health problems.In females, individuals with high microglia ePGS showed a negative association between systemic inflammation and WM-FA and a positive association between more advantageous environmental conditions and WM-FA. The microglia ePGS in females thus accounted for variations in the influence of the quality of the early environment on WM-FA.Finally, WM-FA slopes mediated the association of microglia ePGS with interpersonal problems and social hostility in females. Our findings suggest the genetic capacity for microglia function as a potential factor underlying differential susceptibility to early life exposuresthrough influences on neurodevelopment.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38383882,

title = {Barriers and Facilitators to High Emergency Department Use Among Patients with Mental Disorders: A Qualitative Investigation},

author = {Marie-Josée Fleury and Armelle Imboua and Guy Grenier},

doi = {10.1007/s10597-024-01239-w},

issn = {1573-2789},

year  = {2024},

date = {2024-07-01},

journal = {Community Ment Health J},

volume = {60},

number = {5},

pages = {869--884},

abstract = {This qualitative study explored reasons for high emergency department (ED) use (3 + visits/year) among 299 patients with mental disorders (MD) recruited in four ED in Quebec, Canada. A conceptual framework including healthcare system and ED organizational features, patient profiles, and professional practice guided the content analysis. Results highlighted insufficient access to and inadequacy of outpatient care. While some patients were quite satisfied with ED care, most criticized the lack of referrals or follow-up care. Patient profiles justifying high ED use were strongly associated with health and social issues perceived as needing immediate care. The main barriers in professional practice involved lack of MD expertise among primary care clinicians, and insufficient follow-up by psychiatrists in response to patient needs. Collaboration with outpatient care may be prioritized to reduce high ED use and improve ED interventions by strengthening the discharge process, and increasing access to outpatient care.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38608458,

title = {Degeneration in Nucleus basalis of Meynert signals earliest stage of Alzheimer's disease progression},

author = {Neda Shafiee and Vladimir Fonov and Mahsa Dadar and R Nathan Spreng and D Louis Collins},

doi = {10.1016/j.neurobiolaging.2024.03.003},

issn = {1558-1497},

year  = {2024},

date = {2024-07-01},

journal = {Neurobiol Aging},

volume = {139},

pages = {54--63},

abstract = {Nucleus Basalis of Meynert (NbM), a crucial source of cholinergic projection to the entorhinal cortex (EC) and hippocampus (HC), has shown sensitivity to neurofibrillary degeneration in the early stages of Alzheimer's Disease. Using deformation-based morphometry (DBM) on up-sampled MRI scans from 1447 Alzheimer's Disease Neuroimaging Initiative participants, we aimed to quantify NbM degeneration along the disease trajectory. Results from cross-sectional analysis revealed significant differences of NbM volume between cognitively normal and early mild cognitive impairment cohorts, confirming recent studies suggesting that NbM degeneration happens before degeneration in the EC or HC. Longitudinal linear mixed-effect models were then used to compare trajectories of volume change after realigning all participants into a common timeline based on their cognitive decline. Results indicated the earliest deviations in NbM volumes from the cognitively healthy trajectory, challenging the prevailing idea that Alzheimer's originates in the EC. Converging evidence from cross-sectional and longitudinal models suggest that the NbM may be a focal target of early AD progression, which is often obscured by normal age-related decline.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38754313,

title = {Sociodemographic and clinical correlates of hallucinations in patients entering an early intervention program for first episode psychosis},

author = {Samantha Aversa and Joseph Ghanem and Gili Grunfeld and Ann-Catherine Lemonde and Ashok Malla and Srividya Iyer and Ridha Joober and Martin Lepage and Jai Shah},

doi = {10.1016/j.schres.2024.04.026},

issn = {1573-2509},

year  = {2024},

date = {2024-07-01},

journal = {Schizophr Res},

volume = {269},

pages = {86--92},

abstract = {Hallucinations are a core feature of psychosis, and their severity during the acute phase of illness is associated with a range of poor outcomes. Various clinical and sociodemographic factors may predict hallucinations and other positive psychotic symptoms in first episode psychosis (FEP). Despite this, the precise factors associated with hallucinations at first presentation to an early intervention service have not been extensively researched. Through detailed interviews and chart reviews, we investigated sociodemographic and clinical predictors in 636 minimally-medicated patients who entered PEPP-Montréal, an early intervention service for FEP, between 2003 and 2018. Hallucinations were measured using the Scale for the Assessment of Positive Symptoms (SAPS), while negative symptoms were assessed using the Scale for the Assessment of Negative symptoms (SANS). Depressive symptoms were evaluated through the Calgary Depression Scale for Schizophrenia (CDSS), and anxiety symptoms via the Hamilton Rating Scale for Anxiety (HAS). A majority (n = 381, 59.9 %) of the sample presented with clinically significant hallucinations (SAPS global hallucinations score ≥ 3) at program entry. These patients had an earlier age at onset, fewer years of education, and a higher severity of delusions, depression and negative symptoms than those without clinical-level hallucinations. These results suggest that individuals with clinically significant hallucinations at admission tend to be younger and have a greater overall symptom burden. This makes it especially important to monitor hallucinations alongside delusions, depression and negative symptoms in order to identify who might benefit from targeted interventions. The implications of these findings for early intervention and person-centered care are discussed.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38815437,

title = {Designing and implementing a physical exercise intervention for people with first episode psychosis using experience-based co-design: A pilot study from Chennai, India},

author = {U Vijayalakshmi and R Padmavati and Vijaya Raghavan and Sangeetha Chandrasekaran and Greeshma Mohan and Jothilakshmi Durairaj and Graeme Currie and Richard Lilford and Vivek Furtado and Jason Madan and Maximilian Birchwood and Caroline Meyer and Mamta Sood and Rakesh Chadda and Mohapradeep Mohan and Jai Shah and Sujit John and Srividya N Iyer and R Thara and Swaran Singh},

doi = {10.1016/j.ajp.2024.104072},

issn = {1876-2026},

year  = {2024},

date = {2024-07-01},

journal = {Asian J Psychiatr},

volume = {97},

pages = {104072},

abstract = {BACKGROUND: Physical exercise can improve outcomes for people with first-episode psychosis (FEP). Co-designing physical exercise interventions with end users has the potential to enhance their acceptability, feasibility, and long-term viability. This study's objective was to use experience-based co-design (EBCD) methodology to develop a physical exercise intervention for FEP, and pilot test it.nnMETHODS: The study was conducted at the Schizophrenia Research Foundation's FEP program in Chennai, India. Participants(N=36) were individuals with FEP and their caregivers, mental health professionals (MHPs, and physical training experts. EBCD methodology included one-to-one interviews, focus group discussions, joint conferences, and co-design workshops. Two instructional videos were developed. Twelve FEP patients engaged in physical exercise with help of the videos over three months. They were followed up through weekly phone calls and in-person interviews to capture data on regularity, frequency, location of exercise, and comfort levels.nnRESULTS: Several touch points emerged from the interviews, focus groups, and joint meetings including lack of motivation, knowledge about physical exercise; differing perspectives about physical exercise; limited resource, and time constraints. Two instructional videos demonstrating activities for participants incorporated strategies that addressed these touch points. Pilot data indicated that participants engaged with the physical exercise intervention over 3 months.nnCONCLUSION: This was the first study to use co-design methodology to design a physical exercise intervention for first-episode psychosis. The intervention may have therefore been responsive to stakeholder needs and preferences. Results of this study highlight the potential of co-design in designing and adapting interventions. There is need for rigorous testing with larger samples.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38357733,

title = {Enlarged pituitary gland volume: a possible state rather than trait marker of psychotic disorders},

author = {Synthia Guimond and Ahmad Alftieh and Gabriel A Devenyi and Luke Mike and M Mallar Chakravarty and Jai L Shah and David A Parker and John A Sweeney and Godfrey Pearlson and Brett A Clementz and Carol A Tamminga and Matcheri Keshavan},

doi = {10.1017/S003329172300380X},

issn = {1469-8978},

year  = {2024},

date = {2024-06-01},

journal = {Psychol Med},

volume = {54},

number = {8},

pages = {1835--1843},

abstract = {BACKGROUND: Enlarged pituitary gland volume could be a marker of psychotic disorders. However, previous studies report conflicting results. To better understand the role of the pituitary gland in psychosis, we examined a large transdiagnostic sample of individuals with psychotic disorders.nnMETHODS: The study included 751 participants (174 with schizophrenia, 114 with schizoaffective disorder, 167 with psychotic bipolar disorder, and 296 healthy controls) across six sites in the Bipolar-Schizophrenia Network on Intermediate Phenotypes consortium. Structural magnetic resonance images were obtained, and pituitary gland volumes were measured using the MAGeT brain algorithm. Linear mixed models examined between-group differences with controls and among patient subgroups based on diagnosis, as well as how pituitary volumes were associated with symptom severity, cognitive function, antipsychotic dose, and illness duration.nnRESULTS: Mean pituitary gland volume did not significantly differ between patients and controls. No significant effect of diagnosis was observed. Larger pituitary gland volume was associated with greater symptom severity ( = 13.61,  = 0.0002), lower cognitive function ( = 4.76,  = 0.03), and higher antipsychotic dose ( = 5.20,  = 0.02). Illness duration was not significantly associated with pituitary gland volume. When all variables were considered, only symptom severity significantly predicted pituitary gland volume ( = 7.54,  = 0.006).nnCONCLUSIONS: Although pituitary volumes were not increased in psychotic disorders, larger size may be a marker associated with more severe symptoms in the progression of psychosis. This finding helps clarify previous inconsistent reports and highlights the need for further research into pituitary gland-related factors in individuals with psychosis.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38413700,

title = {The effects of acute social ostracism on subsequent snacking behavior and future body mass index in children},

author = {Aimee E Pink and Reena Teo and Bob Chua and Fabian Kong and Ranjani Nadarajan and Jia Ying Pei and Charmaine H Y Tan and Jia Ying Toh and Yap-Seng Chong and Kok Hian Tan and Fabian Yap and Michael J Meaney and Birit F P Broekman and Bobby K Cheon},

doi = {10.1038/s41366-024-01489-4},

issn = {1476-5497},

year  = {2024},

date = {2024-06-01},

journal = {Int J Obes (Lond)},

volume = {48},

number = {6},

pages = {867--875},

abstract = {BACKGROUND/OBJECTIVES: Ostracism may lead to increased food intake, yet it is unclear whether greater reactivity to ostracism contributes to higher body mass index (BMI). We investigated whether children who exhibited greater stress to social exclusion subsequently consume more energy and whether this predicts BMI 6- and 18-months later.nnSUBJECTS/METHODS: Children (8.5 years-old) (N = 262, males = 50.4%; Chinese = 58.4%) completed a laboratory-based manipulation of social exclusion (the Cyberball task) prior to an ad-libitum snack. Heart rate variability (HRV) was measured during the inclusion and exclusion conditions and proportionate changes were calculated as a physiological measure of exclusion-related stress. Social anxiety and social-emotional assets were also measured as moderators.nnRESULTS: Greater stress (as measured physiologically or by self-report) did not directly, or indirectly via energy intake, predict later BMI (at 9- and 10-years). However, among children reporting higher social anxiety, greater stress as measured by proportionate changes in HRV was associated with increased energy intake (B = 532.88, SE = 226.49, t(255) = 2.35, [CI = 86.85,978.92]). A significant moderated mediation was also observed (index: (b = 0.01, SE = 0.01, [CI = 0.001, 0.036]), such that among children reporting higher social anxiety, greater stress from social exclusion predicted increased energy intake from a subsequent snack, which in turn predicted higher BMI 1.5 years later.nnCONCLUSION: This prospective study suggests that a pattern of greater snack intake in response to heightened vulnerability to the effects of ostracism may contribute to increases in child BMI scores.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid37977417,

title = {Independent Prediction of Child Psychiatric Symptoms by Maternal Mental Health and Child Polygenic Risk Scores},

author = {Lawrence M Chen and Irina Pokhvisneva and Marius Lahti-Pulkkinen and Tuomas Kvist and Jessie R Baldwin and Carine Parent and Patricia P Silveira and Jari Lahti and Katri Räikkönen and Vivette Glover and Thomas G O'Connor and Michael J Meaney and Kieran J O'Donnell},

doi = {10.1016/j.jaac.2023.08.018},

issn = {1527-5418},

year  = {2024},

date = {2024-06-01},

journal = {J Am Acad Child Adolesc Psychiatry},

volume = {63},

number = {6},

pages = {640--651},

abstract = {OBJECTIVE: Prenatal maternal symptoms of depression and anxiety are associated with an increased risk for child socioemotional and behavioral difficulties, supporting the fetal origins of mental health hypothesis. However, to date, studies have not considered specific genomic risk as a possible confound.nnMETHOD: The Avon Longitudinal Study of Parents and Children (ALSPAC) cohort (n = 5,546) was used to test if child polygenic risk score for attention-deficit/hyperactivity disorder (ADHD), schizophrenia, or depression confounds or modifies the impact of prenatal maternal depression and anxiety on child internalizing, externalizing, and total emotional/behavioral symptoms from age 4 to 16 years. Longitudinal child and adolescent symptom data were analyzed in the ALSPAC cohort using generalized estimating equations. Replication analyses were done in an independent cohort (Prevention of Preeclampsia and Intrauterine Growth Restriction [PREDO] cohort; n = 514) from Finland, which provided complementary measures of maternal mental health and child psychiatric symptoms.nnRESULTS: Maternal depression and anxiety and child polygenic risk scores independently and additively predicted behavioral and emotional symptoms from childhood through mid-adolescence. There was a robust prediction of child and adolescent symptoms from both prenatal maternal depression (generalized estimating equation estimate = 0.093, 95% CI 0.065-0.121, p = 2.66 × 10) and anxiety (generalized estimating equation estimate = 0.065, 95% CI 0.037-0.093, p = 1.62 × 10) after adjusting for child genomic risk for mental disorders. There was a similar independent effect of maternal depression (B = 0.156, 95% CI 0.066-0.246, p = .001) on child symptoms in the PREDO cohort. Genetically informed sensitivity analyses suggest that shared genetic risk only partially explains the reported association between prenatal maternal depression and offspring mental health.nnCONCLUSION: These findings highlight the genomic contribution to the fetal origins of mental health hypothesis and further evidence that prenatal maternal depression and anxiety are robust in utero risks for child and adolescent psychiatric symptoms.nnPLAIN LANGUAGE SUMMARY: Depression and anxiety affect approximately 15% of pregnant women, and children exposed to maternal depression or anxiety during pregnancy are at higher risk of developing mental health problems. However, the degree to which shared genetics explains the association between maternal and child mental health is unknown. In this study the authors generated polygenic risk scores (PRS), which provide a single measure of genetic risk for complex traits, to investigate the impact of shared genetic risk on the development of childhood mental health problems. Utilizing two longitudinal studies (n = 6,060), the authors found that PRS only partially explained the association between prenatal maternal depression and childhood mental health problems. These analyses show prenatal maternal depression remained a significant predictor of childhood mental health problems after accounting for shared genetic risk, further highlighting that prenatal maternal mental health is a robust predictor of child and adolescent mental health problems.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid37994452,

title = {Association of cortical gyrification, white matter microstructure, and phenotypic profile in medication-naïve obsessive-compulsive disorder},

author = {Jianyu Li and Jian Cheng and Lei Yang and Qihui Niu and Yuanchao Zhang and Lena Palaniyappan},

doi = {10.1017/S0033291723003422},

issn = {1469-8978},

year  = {2024},

date = {2024-06-01},

journal = {Psychol Med},

volume = {54},

number = {8},

pages = {1573--1579},

abstract = {BACKGROUND: Obsessive-compulsive disorder (OCD) is thought to arise from dysconnectivity among interlinked brain regions resulting in a wide spectrum of clinical manifestations. Cortical gyrification, a key morphological feature of human cerebral cortex, has been considered associated with developmental connectivity in early life. Monitoring cortical gyrification alterations may provide new insights into the developmental pathogenesis of OCD.nnMETHODS: Sixty-two medication-naive patients with OCD and 59 healthy controls (HCs) were included in this study. Local gyrification index (LGI) was extracted from T1-weighted MRI data to identify the gyrification changes in OCD. Total distortion (splay, bend, or twist of fibers) was calculated using diffusion-weighted MRI data to examine the changes in white matter microstructure in patients with OCD.nnRESULTS: Compared with HCs, patients with OCD showed significantly increased LGI in bilateral medial frontal gyrus and the right precuneus, where the mean LGI was positively correlated with anxiety score. Patients with OCD also showed significantly decreased total distortion in the body, genu, and splenium of the corpus callosum (CC), where the average distortion was negatively correlated with anxiety scores. Intriguingly, the mean LGI of the affected cortical regions was significantly correlated with the mean distortion of the affected white matter tracts in patients with OCD.nnCONCLUSIONS: We demonstrated associations among increased LGI, aberrant white matter geometry, and higher anxiety in patients with OCD. Our findings indicate that developmental dysconnectivity-driven alterations in cortical folding are one of the neural substrates underlying the clinical manifestations of OCD.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38478216,

title = {Mental health of Canadian youth: A systematic review and meta-analysis of studies examining changes in depression, anxiety, and suicide-related outcomes during the COVID-19 pandemic},

author = {Marie-Claude Geoffroy and Nicholas Chadi and Samantha Bouchard and Julia Fuoco and Elise Chartrand and Tianna Loose and Anthony Sciola and Jill T Boruff and Srividya N Iyer and Ying Sun and Jean-Philippe Gouin and Sylvana M Côté and Brett D Thombs},

doi = {10.17269/s41997-024-00865-x},

issn = {1920-7476},

year  = {2024},

date = {2024-06-01},

journal = {Can J Public Health},

volume = {115},

number = {3},

pages = {408--424},

abstract = {OBJECTIVES: This systematic review and meta-analysis aims to describe Canadian youth mental health during the COVID-19 pandemic, focusing on changes in anxiety and depressive symptoms and suicidality.nnMETHODS: We searched four databases up to February 2023 for longitudinal or repeated cross-sectional studies reporting on changes in depressive and anxiety symptoms, suicidality, or related services utilization among young people under 25 years old residing in Canada during the COVID-19 pandemic. Random-effects meta-analyses were performed for studies comparing depressive and anxiety symptoms from before to during the first, second, and third COVID-19 waves (up to June 2021), and between COVID-19 waves. Other studies were described narratively. Risk of bias was assessed using an adapted Joanna Briggs Institute Checklist.nnSYNTHESIS: Of the 7916 records screened, 35 articles met inclusion criteria for this review. Included studies were highly heterogeneous in design, population, and type of change investigated, and many had a high risk of bias. The meta-analyses found that depressive symptoms worsened minimally from pre-pandemic to wave 1 but returned to pre-pandemic levels by wave 2. Anxiety symptoms were broadly comparable from pre-pandemic to waves 1 and 2 but worsened from waves 1 to 3 and from pre-pandemic to wave 1 for girls. The narrative review included several studies that provided inconclusive evidence of increases in services utilization.nnCONCLUSION: The current evidence is limited and highly heterogeneous, making it insufficient to draw definitive conclusions regarding the short- to medium-term impact of the pandemic on youth mental health in Canada. Obtaining better mental health surveillance among Canadian youth is imperative.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38486790,

title = {Using virtual reality to improve verbal episodic memory in schizophrenia: A proof-of-concept trial},

author = {Bryce J M Bogie and Chelsea Noël and Feng Gu and Sébastien Nadeau and Cecelia Shvetz and Hassan Khan and Marie-Christine Rivard and Stéphane Bouchard and Martin Lepage and Synthia Guimond},

doi = {10.1016/j.scog.2024.100305},

issn = {2215-0013},

year  = {2024},

date = {2024-06-01},

journal = {Schizophr Res Cogn},

volume = {36},

pages = {100305},

abstract = {BACKGROUND: Schizophrenia is associated with impairments in verbal episodic memory. Strategy for Semantic Association Memory (SESAME) training represents a promising cognitive remediation program to improve verbal episodic memory. Virtual reality (VR) may be a novel tool to increase the ecological validity and transfer of learned skills of traditional cognitive remediation programs. The present proof-of-concept study aimed to assess the feasibility, acceptability, and preliminary efficacy of a VR-based cognitive remediation module inspired by SESAME principles to improve the use of verbal episodic memory strategies in schizophrenia.nnMETHODS: Thirty individuals with schizophrenia/schizoaffective disorder completed this study. Participants were randomized to either a VR-based verbal episodic memory training condition inspired by SESAME principles (intervention group) or an active control condition (control group). In the training condition, a coach taught semantic encoding strategies (active rehearsal and semantic clustering) to help participants remember restaurant orders in VR. In the active control condition, participants completed visuospatial puzzles in VR. Attrition rate, participant experience ratings, and cybersickness questionnaires were used to assess feasibility and acceptability. Trial 1 of the Hopkins Verbal Learning Test - Revised was administered pre- and post-intervention to assess preliminary efficacy.nnRESULTS: Feasibility was demonstrated by a low attrition rate (5.88 %), and acceptability was demonstrated by limited cybersickness and high levels of enjoyment. Although the increase in the number of semantic clusters used following the module did not reach conventional levels of statistical significance in the intervention group, it demonstrated a notable trend with a medium effect size ( = 1.48,  = 0.15,  = 0.54), in contrast to the control group where it remained stable ( = 0.36,  = 0.72,  = 0.13). These findings were similar for the semantic clustering ratio in the intervention ( = 1.61,  = 0.12,  = 0.59) and control ( = 0.36,  = 0.72,  = 0.13) groups. There was no significant change in the number of recalled words in either group following VR immersion.nnDISCUSSION: This VR intervention was feasible, acceptable, and may be useful for improving the use of semantic encoding strategies. These findings support the use of more ecological approaches for the treatment of cognitive impairments in schizophrenia, such as VR-based cognitive remediation.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38526098,

title = {Longer sleep duration and neuroinflammation in at-risk elderly with a parental history of Alzheimer's disease},

author = {Andrée-Ann Baril and Cynthia Picard and Anne Labonté and Erlan Sanchez and Catherine Duclos and Béry Mohammediyan and John C S Breitner and Sylvia Villeneuve and Judes Poirier and },

doi = {10.1093/sleep/zsae081},

issn = {1550-9109},

year  = {2024},

date = {2024-06-01},

journal = {Sleep},

volume = {47},

number = {6},

abstract = {STUDY OBJECTIVES: Although short sleep could promote neurodegeneration, long sleep may be a marker of ongoing neurodegeneration, potentially as a result of neuroinflammation. The objective was to evaluate sleep patterns with age of expected Alzheimer's disease (AD) onset and neuroinflammation.nnMETHODS: We tested 203 dementia-free participants (68.5 ± 5.4 years old, 78M). The PREVENT-AD cohort includes older persons with a parental history of AD whose age was nearing their expected AD onset. We estimated expected years to AD onset by subtracting the participants' age from their parent's at AD dementia onset. We extracted actigraphy sleep variables of interest (times of sleep onset and morning awakening, time in bed, sleep efficiency, and sleep duration) and general profiles (sleep fragmentation, phase delay, and hypersomnia). Cerebrospinal fluid (CSF) inflammatory biomarkers were assessed with OLINK multiplex technology.nnRESULTS: Proximity to, or exceeding, expected age of onset was associated with a sleep profile suggestive of hypersomnia (longer sleep and later morning awakening time). This hypersomnia sleep profile was associated with higher CSF neuroinflammatory biomarkers (IL-6, MCP-1, and global score). Interaction analyses revealed that some of these sleep-neuroinflammation associations were present mostly in those closer/exceeding the age of expected AD onset, APOE4 carriers, and those with better memory performance.nnCONCLUSIONS: Proximity to, or exceeding, parental AD dementia onset was associated with a longer sleep pattern, which was related to elevated proinflammatory CSF biomarkers. We speculate that longer sleep may serve a compensatory purpose potentially triggered by neuroinflammation as individuals are approaching AD onset. Further studies should investigate whether neuroinflammatory-triggered long sleep duration could mitigate cognitive deficits.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38584240,

title = {Profiles of Permanent Supportive Housing Residents Related to Their Housing Conditions, Service Use, and Associated Sociodemographic and Clinical Characteristics},

author = {Marie-Josée Fleury and Bahram Armoon},

doi = {10.1007/s11126-024-10071-0},

issn = {1573-6709},

year  = {2024},

date = {2024-06-01},

journal = {Psychiatr Q},

volume = {95},

number = {2},

pages = {203--219},

abstract = {As permanent supportive housing (PSH) is the main strategy promoted to reduce homelessness, understanding how PSH resident profiles may be differentiated is crucial to the optimization of PSH implementation - and a subject that hasn't been studied yet. This study identified PSH resident profiles based on their housing conditions and service use, associated with their sociodemographic and clinical characteristics. In 2020-2021, 308 PSH residents from Quebec (Canada) were interviewed, with K-means cluster analysis produced to identify profiles and subsequent analyses to compare profiles and PSH resident characteristics. Of the three profiles identified, Profiles 1 and 2 (70% of sample) showed moderate or poor housing, neighborhood, and health conditions, and moderate or high unmet care needs and service use. Besides their "moderate" conditions, Profile 1 residents (52%) reported being in PSH for more than two years and being less educated. With the "worst" conditions and high service use, Profile 2 (18%) included younger individuals, while Profile 3 (30%) showed the "best" conditions and integrated individuals with more protective determinants (e.g., few in foster care, homelessness at older age, more self-esteem), with a majority living in single-site PSH and reporting higher satisfaction with support and community-based services. Profiles 1 and 2 may be provided with more psychosocial, crisis, harm reduction, and empowerment interventions, and peer helper support. Profile 2 may benefit from more intensive and integrated care, and better housing conditions. Continuous PSH may be sustained for Profile 3, with regular monitoring of service satisfaction and met needs.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38917846,

title = {Integrative Genetic Variation, DNA Methylation, and Gene Expression Analysis of Escitalopram and Aripiprazole Treatment Outcomes in Depression: A CAN-BIND-1 Study},

author = {Farhana Islam and Amanda Lisoway and Edward S Oh and Laura M Fiori and Leen Magarbeh and Samar S M Elsheikh and Helena K Kim and Stefan Kloiber and James L Kennedy and Benicio N Frey and Roumen Milev and Claudio N Soares and Sagar V Parikh and Franca Placenza and Stefanie Hassel and Valerie H Taylor and Francesco Leri and Pierre Blier and Rudolf Uher and Faranak Farzan and Raymond W Lam and Gustavo Turecki and Jane A Foster and Susan Rotzinger and Sidney H Kennedy and Daniel J Müller},

doi = {10.1055/a-2313-9979},

issn = {1439-0795},

year  = {2024},

date = {2024-06-01},

journal = {Pharmacopsychiatry},

abstract = {INTRODUCTION: Little is known about the interplay between genetics and epigenetics on antidepressant treatment (1) response and remission, (2) side effects, and (3) serum levels. This study explored the relationship among single nucleotide polymorphisms (SNPs), DNA methylation (DNAm), and mRNA levels of four pharmacokinetic genes, , , , and , and its effect on these outcomes.nnMETHODS: The Canadian Biomarker Integration Network for Depression-1 dataset consisted of 177 individuals with major depressive disorder treated for 8 weeks with escitalopram (ESC) followed by 8 weeks with ESC monotherapy or augmentation with aripiprazole. DNAm quantitative trait loci (mQTL), identified by SNP-CpG associations between 20 SNPs and 60 CpG sites in whole blood, were tested for associations with our outcomes, followed by causal inference tests (CITs) to identify methylation-mediated genetic effects.nnRESULTS: Eleven SNP-CpG pairs (q<0.05) constituting four unique SNPs were identified. Although no significant associations were observed between mQTLs and response/remission,  rs4244285 was associated with treatment-related weight gain (=0.027) and serum concentrations of ESC (<0.001). Between weeks 2-4, 6.7% and 14.9% of those with *1/*1 (normal metabolizers) and *1/*2 (intermediate metabolizers) genotypes, respectively, reported ≥2 lbs of weight gain. In contrast, the *2/*2 genotype (poor metabolizers) did not report weight gain during this period and demonstrated the highest ESC concentrations. CITs did not indicate that these effects were epigenetically mediated.nnDISCUSSION: These results elucidate functional mechanisms underlying the established associations between  rs4244285 and ESC pharmacokinetics. This mQTL SNP as a marker for antidepressant-related weight gain needs to be further explored.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38916585,

title = {Circadian Control of the Response of Macrophages to Plasmodium Spp.-Infected Red Blood Cells},

author = {Priscilla Carvalho Cabral and Vincent R Richard and Christoph H Borchers and Martin Olivier and Nicolas Cermakian},

doi = {10.4049/immunohorizons.2400021},

issn = {2573-7732},

year  = {2024},

date = {2024-06-01},

journal = {Immunohorizons},

volume = {8},

number = {6},

pages = {442--456},

abstract = {Malaria is a serious vector-borne disease characterized by periodic episodes of high fever and strong immune responses that are coordinated with the daily synchronized parasite replication cycle inside RBCs. As immune cells harbor an autonomous circadian clock that controls various aspects of the immune response, we sought to determine whether the intensity of the immune response to Plasmodium spp., the parasite causing malaria, depends on time of infection. To do this, we developed a culture model in which mouse bone marrow-derived macrophages are stimulated with RBCs infected with Plasmodium berghei ANKA (iRBCs). Lysed iRBCs, but not intact iRBCs or uninfected RBCs, triggered an inflammatory immune response in bone marrow-derived macrophages. By stimulating at four different circadian time points (16, 22, 28, or 34 h postsynchronization of the cells' clock), 24-h rhythms in reactive oxygen species and cytokines/chemokines were found. Furthermore, the analysis of the macrophage proteome and phosphoproteome revealed global changes in response to iRBCs that varied according to circadian time. This included many proteins and signaling pathways known to be involved in the response to Plasmodium infection. In summary, our findings show that the circadian clock within macrophages determines the magnitude of the inflammatory response upon stimulation with ruptured iRBCs, along with changes of the cell proteome and phosphoproteome.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38908214,

title = {Patient- and family-reported experiences of their treating teams in early psychosis services in Chennai, India and Montreal, Canada},

author = {Aarati Taksal and Greeshma Mohan and Ashok Malla and Daniel Rabouin and MaryAnne Levasseur and Thara Rangaswamy and Ramachandran Padmavati and Ridha Joober and Howard C Margolese and Norbert Schmitz and Srividya N Iyer},

doi = {10.1016/j.ajp.2024.104118},

issn = {1876-2026},

year  = {2024},

date = {2024-06-01},

journal = {Asian J Psychiatr},

volume = {98},

pages = {104118},

abstract = {BACKGROUND: Cross-cultural psychosis research has mostly focused on outcomes, rather than patient and family experiences. Therefore, our aim was to examine differences in patients' and families' experiences of their treating teams in early intervention services for psychosis in Chennai, India [low- and middle-income country] and Montreal, Canada [high-income country].nnMETHODS: Patients (165 in Chennai, 128 in Montreal) and their families (135 in Chennai, 110 in Montreal) completed Show me you care, a patient- and family-reported experience measure, after Months 3, 12, and 24 in treatment. The measure assesses the extent to which patients and families view treating teams as being supportive. A linear mixed model with longitudinal data from patient and family dyads was used to test the effect of site (Chennai, Montreal), stakeholder (patient, family), and time on Show me you care scores. This was followed by separate linear mixed effect models for patients and families with age and gender, as well as symptom severity and functioning as time-varying covariates.nnRESULTS: As hypothesized, Chennai patients and families reported more supportive behaviours from their treating teams (β=4.04; β= 9, respectively) than did Montreal patients (Intercept =49.6) and families (Intercept=42.45). Higher symptom severity over follow-up was associated with patients reporting lower supportive behaviours from treating teams. Higher levels of positive symptoms (but lower levels of negative symptoms) over follow-up were associated with families reporting lower supportive behaviours from treating teams. There was no effect of time, age, gender and functioning.nnCONCLUSIONS: The levels to which treating teams are perceived as supportive may reflect culturally shaped attitudes (e.g., warmer attitudes towards healthcare providers in India vis-à-vis Canada) and actual differences in how supportive treating teams are, which too may be culturally shaped. Being expected to be more involved in treatment, Chennai families may receive more attention and support, which may further reinforce their involvement. Across contexts, those who improve over follow-up may see their treating teams more positively.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38906883,

title = {Development of a differential treatment selection model for depression on consolidated and transformed clinical trial datasets},

author = {Kelly Perlman and Joseph Mehltretter and David Benrimoh and Caitrin Armstrong and Robert Fratila and Christina Popescu and Jingla-Fri Tunteng and Jerome Williams and Colleen Rollins and Grace Golden and Gustavo Turecki},

doi = {10.1038/s41398-024-02970-4},

issn = {2158-3188},

year  = {2024},

date = {2024-06-01},

journal = {Transl Psychiatry},

volume = {14},

number = {1},

pages = {263},

abstract = {Major depressive disorder (MDD) is the leading cause of disability worldwide, yet treatment selection still proceeds via "trial and error". Given the varied presentation of MDD and heterogeneity of treatment response, the use of machine learning to understand complex, non-linear relationships in data may be key for treatment personalization. Well-organized, structured data from clinical trials with standardized outcome measures is useful for training machine learning models; however, combining data across trials poses numerous challenges. There is also persistent concern that machine learning models can propagate harmful biases. We have created a methodology for organizing and preprocessing depression clinical trial data such that transformed variables harmonized across disparate datasets can be used as input for feature selection. Using Bayesian optimization, we identified an optimal multi-layer dense neural network that used data from 21 clinical and sociodemographic features as input in order to perform differential treatment benefit prediction. With this combined dataset of 5032 individuals and 6 drugs, we created a differential treatment benefit prediction model. Our model generalized well to the held-out test set and produced similar accuracy metrics in the test and validation set with an AUC of 0.7 when predicting binary remission. To address the potential for bias propagation, we used a bias testing performance metric to evaluate the model for harmful biases related to ethnicity, age, or sex. We present a full pipeline from data preprocessing to model validation that was employed to create the first differential treatment benefit prediction model for MDD containing 6 treatment options.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38905724,

title = {Protocol-based assessment and management of first episode psychosis: Comparison of short and medium-term outcomes in psychopathology, quality of life, functioning and family burden across two sites in India},

author = {Rakesh K Chadda and Mamta Sood and Nishtha Chawla and R Padmavati and Rangaswamy Thara and Vijaya Raghavan and Tulika Shukla and Vaibhav Patil and Mahadev Singh Sen and Mohapradeep Mohan and Srividya Iyer and Jai Shah and Jason Madan and Max Birchwood and Caroline Meyer and R J Lilford and Vivek Furtado and Graeme Currie and Swaran P Singh},

doi = {10.1016/j.ajp.2024.104103},

issn = {1876-2026},

year  = {2024},

date = {2024-06-01},

journal = {Asian J Psychiatr},

volume = {98},

pages = {104103},

abstract = {BACKGROUND: Standard assessment and management protocols exist for first episode psychosis (FEP) in high income countries. Due to cultural and resource differences, these need to be modified for application in low-and middle-income countries.nnAIMS: To assess the applicability of standard assessment and management protocols across two cohorts of FEP patients in North and South India by examining trajectories of psychopathology, functioning, quality of life and family burden in both.nnMETHOD: FEP patients at two sites (108 at AIIMS, North India, and 115 at SCARF, South India) were assessed using structured instruments at baseline, 3, 6 and 12 months. Standard management protocols consisted of treatment with antipsychotics and psychoeducation for patients and their families. Generalised estimating equation (GEE) modelling was carried out to test for changes in outcomes both across and between sites at follow-up.nnRESULTS: There was an overall significant improvement in both cohorts for psychopathology and other outcome measures. The trajectories of improvement differed between the two sites with steeper improvement in non-affective psychosis in the first three months at SCARF, and affective symptoms in the first three months at AIIMS. The reduction in family burden and improvement in quality of life were greater at AIIMS than at SCARF during the first three months.nnCONCLUSIONS: Despite variations in cultural contexts and norms, it is possible to implement FEP standard assessment and management protocols in North and South India. Preliminary findings indicate that FEP services lead to significant improvements in psychopathology, functioning, quality of life, and family burden within these contexts.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38878300,

title = {Network enrichment significance testing in brain-phenotype association studies},

author = {Sarah M Weinstein and Simon N Vandekar and Bin Li and Aaron F Alexander-Bloch and Armin Raznahan and Mingyao Li and Raquel E Gur and Ruben C Gur and David R Roalf and Min Tae M Park and Mallar Chakravarty and Erica B Baller and Kristin A Linn and Theodore D Satterthwaite and Russell T Shinohara},

doi = {10.1002/hbm.26714},

issn = {1097-0193},

year  = {2024},

date = {2024-06-01},

journal = {Hum Brain Mapp},

volume = {45},

number = {8},

pages = {e26714},

abstract = {Functional networks often guide our interpretation of spatial maps of brain-phenotype associations. However, methods for assessing enrichment of associations within networks of interest have varied in terms of both scientific rigor and underlying assumptions. While some approaches have relied on subjective interpretations, others have made unrealistic assumptions about spatial properties of imaging data, leading to inflated false positive rates. We seek to address this gap in existing methodology by borrowing insight from a method widely used in genetics research for testing enrichment of associations between a set of genes and a phenotype of interest. We propose network enrichment significance testing (NEST), a flexible framework for testing the specificity of brain-phenotype associations to functional networks or other sub-regions of the brain. We apply NEST to study enrichment of associations with structural and functional brain imaging data from a large-scale neurodevelopmental cohort study.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38874967,

title = {Threat- and Reward-Related Brain Circuitry, Perceived Stress, and Anxiety in Adolescents During the COVID-19 Pandemic: A Longitudinal Investigation},

author = {Lauren R Borchers and Anthony J Gifuni and Tiffany C Ho and Jaclyn S Kirshenbaum and Ian H Gotlib},

doi = {10.1093/scan/nsae040},

issn = {1749-5024},

year  = {2024},

date = {2024-06-01},

journal = {Soc Cogn Affect Neurosci},

abstract = {The COVID-19 pandemic has been related to heightened anxiety in adolescents. The basolateral amygdala (BLA) and the nucleus accumbens (NAcc) have been implicated in response to stress and may contribute to anxiety. The role of threat- and reward-related circuitry in adolescent anxiety during the COVID-19 pandemic, however, is not clear. Ninety-nine adolescents underwent resting-state fMRI approximately one year before the pandemic. Following shelter-in-place orders, adolescents reported their perceived stress and, one month later, their anxiety. Generalized multivariate analyses identified BLA and NAcc seed-based whole-brain connectivity maps with perceived stress. We examined associations between seed-based connectivity in significant clusters and subsequent anxiety. Perceived stress was associated with bilateral BLA and NAcc connectivity across distributed clusters that included prefrontal, limbic, temporal, and cerebellar regions. Several NAcc connectivity clusters located in ventromedial prefrontal, parahippocampal, and temporal cortices were positively associated with anxiety; whereas NAcc connectivity with the inferior frontal gyrus was negatively associated. BLA connectivity was not associated with anxiety. These results underscore the integrative role of the NAcc in responding to acute stressors and its relation to anxiety in adolescents. Elucidating the involvement of subcortical-cortical circuitry in adolescents' capacity to respond adaptively to environmental challenges can inform treatment approaches for anxiety-related disorders.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38326457,

title = {Two polygenic mouse models of major depressive disorders identify TMEM161B as a potential biomarker of disease in humans},

author = {Malika El Yacoubi and Claire Altersitz and Violaine Latapie and Elari Rizkallah and Sébastien Arthaud and Laure Bougarel and Marcela Pereira and Anne Wierinckx and Wissam El-Hage and Raoul Belzeaux and Gustavo Turecki and Per Svenningsson and Benoît Martin and Joël Lachuer and Jean-Marie Vaugeois and Stéphane Jamain},

doi = {10.1038/s41386-024-01811-8},

issn = {1740-634X},

year  = {2024},

date = {2024-06-01},

journal = {Neuropsychopharmacology},

volume = {49},

number = {7},

pages = {1129--1139},

abstract = {Treatments are only partially effective in major depressive disorders (MDD) but no biomarker exists to predict symptom improvement in patients. Animal models are essential tools in the development of antidepressant medications, but while recent genetic studies have demonstrated the polygenic contribution to MDD, current models are limited to either mimic the effect of a single gene or environmental factor. We developed in the past a model of depressive-like behaviors in mice (H/Rouen), using selective breeding based on behavioral reaction after an acute mild stress in the tail suspension test. Here, we propose a new mouse model of depression (H-TST) generated from a more complex genetic background and based on the same selection process. We first demonstrated that H/Rouen and H-TST mice had similar phenotypes and were more sensitive to glutamate-related antidepressant medications than selective serotonin reuptake inhibitors. We then conducted an exome sequencing on the two mouse models and showed that they had damaging variants in 174 identical genes, which have also been associated with MDD in humans. Among these genes, we showed a higher expression level of Tmem161b in brain and blood of our two mouse models. Changes in TMEM161B expression level was also observed in blood of MDD patients when compared with controls, and after 8-week treatment with duloxetine, mainly in good responders to treatment. Altogether, our results introduce H/Rouen and H-TST as the two first polygenic animal models of MDD and demonstrate their ability to identify biomarkers of the disease and to develop rapid and effective antidepressant medications.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38866253,

title = {Depression-Anxiety Coupling Strength as a predictor of relapse in major depressive disorder: A CAN-BIND wellness monitoring study report},

author = {Abraham Nunes and Barbara Pavlova and Jasmyn E A Cunningham and John-Jose Nuñez and Lena C Quilty and Jane A Foster and Kate L Harkness and Keith Ho and Raymond W Lam and Qingqin S Li and Roumen Milev and Susan Rotzinger and Claudio N Soares and Valerie H Taylor and Gustavo Turecki and Sidney H Kennedy and Benicio N Frey and Frank Rudzicz and Rudolf Uher},

doi = {10.1016/j.jad.2024.06.023},

issn = {1573-2517},

year  = {2024},

date = {2024-06-01},

journal = {J Affect Disord},

volume = {361},

pages = {189--197},

abstract = {BACKGROUND: A critical challenge in the study and management of major depressive disorder (MDD) is predicting relapse. We examined the temporal correlation/coupling between depression and anxiety (called Depression-Anxiety Coupling Strength, DACS) as a predictor of relapse in patients with MDD.nnMETHODS: We followed 97 patients with remitted MDD for an average of 394 days. Patients completed weekly self-ratings of depression and anxiety symptoms using the Quick Inventory of Depressive Symptoms (QIDS-SR) and the Generalized Anxiety Disorder 7-item scale (GAD-7). Using these longitudinal ratings we computed DACS as random slopes in a linear mixed effects model reflecting individual-specific degree of correlation between depression and anxiety across time points. We then tested DACS as an independent variable in a Cox proportional hazards model to predict relapse.nnRESULTS: A total of 28 patients (29 %) relapsed during the follow-up period. DACS significantly predicted confirmed relapse (hazard ratio [HR] 1.5, 95 % CI [1.01, 2.22], p = 0.043; Concordance 0.79 [SE 0.04]). This effect was independent of baseline depressive or anxiety symptoms or their average levels over the follow-up period, and was identifiable more than one month before relapse onset.nnLIMITATIONS: Small sample size, in a single study. Narrow phenotype and comorbidity profiles.nnCONCLUSIONS: DACS may offer opportunities for developing novel strategies for personalized monitoring, early detection, and intervention. Future studies should replicate our findings in larger, diverse patient populations, develop individual patient prediction models, and explore the underlying mechanisms that govern the relationship of DACS and relapse.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38865456,

title = {Neuroimaging epicenters as potential sites of onset of the neuroanatomical pathology in schizophrenia},

author = {Yuchao Jiang and Lena Palaniyappan and Cheng Luo and Xiao Chang and Jie Zhang and Yingying Tang and Tianhong Zhang and Chunbo Li and Enpeng Zhou and Xin Yu and Wei Li and Dongmei An and Dong Zhou and Chu-Chung Huang and Shih-Jen Tsai and Ching-Po Lin and Jingliang Cheng and Jijun Wang and Dezhong Yao and Wei Cheng and Jianfeng Feng and },

doi = {10.1126/sciadv.adk6063},

issn = {2375-2548},

year  = {2024},

date = {2024-06-01},

journal = {Sci Adv},

volume = {10},

number = {24},

pages = {eadk6063},

abstract = {Schizophrenia lacks a clear definition at the neuroanatomical level, capturing the sites of origin and progress of this disorder. Using a network-theory approach called epicenter mapping on cross-sectional magnetic resonance imaging from 1124 individuals with schizophrenia, we identified the most likely "source of origin" of the structural pathology. Our results suggest that the Broca's area and adjacent frontoinsular cortex may be the epicenters of neuroanatomical pathophysiology in schizophrenia. These epicenters can predict an individual's response to treatment for psychosis. In addition, cross-diagnostic similarities based on epicenter mapping over of 4000 individuals diagnosed with neurological, neurodevelopmental, or psychiatric disorders appear to be limited. When present, these similarities are restricted to bipolar disorder, major depressive disorder, and obsessive-compulsive disorder. We provide a comprehensive framework linking schizophrenia-specific epicenters to multiple levels of neurobiology, including cognitive processes, neurotransmitter receptors and transporters, and human brain gene expression. Epicenter mapping may be a reliable tool for identifying the potential onset sites of neural pathophysiology in schizophrenia.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38865039,

title = {Exploring the genetics of lithium response in bipolar disorders},

author = {Marisol Herrera-Rivero and Mazda Adli and Kazufumi Akiyama and Nirmala Akula and Azmeraw T Amare and Raffaella Ardau and Bárbara Arias and Jean-Michel Aubry and Lena Backlund and Frank Bellivier and Antonio Benabarre and Susanne Bengesser and Abesh Kumar Bhattacharjee and Joanna M Biernacka and Armin Birner and Micah Cearns and Pablo Cervantes and Hsi-Chung Chen and Caterina Chillotti and Sven Cichon and Scott R Clark and Francesc Colom and Cristiana Cruceanu and Piotr M Czerski and Nina Dalkner and Franziska Degenhardt and Maria Del Zompo and J Raymond DePaulo and Bruno Etain and Peter Falkai and Ewa Ferensztajn-Rochowiak and Andreas J Forstner and Josef Frank and Louise Frisén and Mark A Frye and Janice M Fullerton and Carla Gallo and Sébastien Gard and Julie S Garnham and Fernando S Goes and Maria Grigoroiu-Serbanescu and Paul Grof and Ryota Hashimoto and Roland Hasler and Joanna Hauser and Urs Heilbronner and Stefan Herms and Per Hoffmann and Liping Hou and Yi-Hsiang Hsu and Stephane Jamain and Esther Jiménez and Jean-Pierre Kahn and Layla Kassem and Tadafumi Kato and John Kelsoe and Sarah Kittel-Schneider and Po-Hsiu Kuo and Ichiro Kusumi and Barbara König and Gonzalo Laje and Mikael Landén and Catharina Lavebratt and Marion Leboyer and Susan G Leckband and Mario Maj and Mirko Manchia and Cynthia Marie-Claire and Lina Martinsson and Michael J McCarthy and Susan L McElroy and Vincent Millischer and Marina Mitjans and Francis M Mondimore and Palmiero Monteleone and Caroline M Nievergelt and Tomas Novák and Markus M Nöthen and Claire O'Donovan and Norio Ozaki and Sergi Papiol and Andrea Pfennig and Claudia Pisanu and James B Potash and Andreas Reif and Eva Reininghaus and Hélène Richard-Lepouriel and Gloria Roberts and Guy A Rouleau and Janusz K Rybakowski and Martin Schalling and Peter R Schofield and Klaus Oliver Schubert and Eva C Schulte and Barbara W Schweizer and Giovanni Severino and Tatyana Shekhtman and Paul D Shilling and Katzutaka Shimoda and Christian Simhandl and Claire M Slaney and Alessio Squassina and Thomas Stamm and Pavla Stopkova and Fabian Streit and Fasil Tekola-Ayele and Anbupalam Thalamuthu and Alfonso Tortorella and Gustavo Turecki and Julia Veeh and Eduard Vieta and Biju Viswanath and Stephanie H Witt and Peter P Zandi and Martin Alda and Michael Bauer and Francis J McMahon and Philip B Mitchell and Marcella Rietschel and Thomas G Schulze and Bernhard T Baune},

doi = {10.1186/s40345-024-00341-y},

issn = {2194-7511},

year  = {2024},

date = {2024-06-01},

journal = {Int J Bipolar Disord},

volume = {12},

number = {1},

pages = {20},

abstract = {BACKGROUND: Lithium (Li) remains the treatment of choice for bipolar disorders (BP). Its mood-stabilizing effects help reduce the long-term burden of mania, depression and suicide risk in patients with BP. It also has been shown to have beneficial effects on disease-associated conditions, including sleep and cardiovascular disorders. However, the individual responses to Li treatment vary within and between diagnostic subtypes of BP (e.g. BP-I and BP-II) according to the clinical presentation. Moreover, long-term Li treatment has been linked to adverse side-effects that are a cause of concern and non-adherence, including the risk of developing chronic medical conditions such as thyroid and renal disease. In recent years, studies by the Consortium on Lithium Genetics (ConLiGen) have uncovered a number of genetic factors that contribute to the variability in Li treatment response in patients with BP. Here, we leveraged the ConLiGen cohort (N = 2064) to investigate the genetic basis of Li effects in BP. For this, we studied how Li response and linked genes associate with the psychiatric symptoms and polygenic load for medical comorbidities, placing particular emphasis on identifying differences between BP-I and BP-II.nnRESULTS: We found that clinical response to Li treatment, measured with the Alda scale, was associated with a diminished burden of mania, depression, substance and alcohol abuse, psychosis and suicidal ideation in patients with BP-I and, in patients with BP-II, of depression only. Our genetic analyses showed that a stronger clinical response to Li was modestly related to lower polygenic load for diabetes and hypertension in BP-I but not BP-II. Moreover, our results suggested that a number of genes that have been previously linked to Li response variability in BP differentially relate to the psychiatric symptomatology, particularly to the numbers of manic and depressive episodes, and to the polygenic load for comorbid conditions, including diabetes, hypertension and hypothyroidism.nnCONCLUSIONS: Taken together, our findings suggest that the effects of Li on symptomatology and comorbidity in BP are partially modulated by common genetic factors, with differential effects between BP-I and BP-II.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38844534,

title = {Shared and unique transcriptomic signatures of antidepressant and probiotics action in the mammalian brain},

author = {Nirmala Arul Rayan and Jonathan Aow and Michelle Gek Liang Lim and Danusa Mar Arcego and Richard Ryan and Nooshin Nourbakhsh and Randriely Merscher Sobreira de Lima and Kelly Craig and Tie Yuan Zhang and Yeek Teck Goh and Alfred Xuyang Sun and Thomas Tompkins and Stéphane Bronner and Sylvie Binda and Josie Diorio and Carine Parent and Michael J Meaney and Shyam Prabhakar},

doi = {10.1038/s41380-024-02619-0},

issn = {1476-5578},

year  = {2024},

date = {2024-06-01},

journal = {Mol Psychiatry},

abstract = {Understanding the shared and divergent mechanisms across antidepressant (AD) classes and probiotics is critical for improving treatment for mood disorders. Here we examine the transcriptomic effects of bupropion (NDRI), desipramine (SNRI), fluoxetine (SSRI) and a probiotic formulation (Lacidofil®) on 10 regions across the mammalian brain. These treatments massively alter gene expression (on average, 2211 differentially expressed genes (DEGs) per region-treatment combination), highlighting the biological complexity of AD and probiotic action. Intersection of DEG sets against neuropsychiatric GWAS loci, sex-specific transcriptomic portraits of major depressive disorder (MDD), and mouse models of stress and depression reveals significant similarities and differences across treatments. Interestingly, molecular responses in the infralimbic cortex, basolateral amygdala and locus coeruleus are region-specific and highly similar across treatments, whilst responses in the Raphe, medial preoptic area, cingulate cortex, prelimbic cortex and ventral dentate gyrus are predominantly treatment-specific. Mechanistically, ADs concordantly downregulate immune pathways in the amygdala and ventral dentate gyrus. In contrast, protein synthesis, metabolism and synaptic signaling pathways are axes of variability among treatments. We use spatial transcriptomics to further delineate layer-specific molecular pathways and DEGs within the prefrontal cortex. Our study reveals complex AD and probiotics action on the mammalian brain and identifies treatment-specific cellular processes and gene targets associated with mood disorders.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38830849,

title = {Neuromodulatory subcortical nucleus integrity is associated with white matter microstructure, tauopathy and APOE status},

author = {Alfie Wearn and Stéfanie A Tremblay and Christine L Tardif and Ilana R Leppert and Claudine J Gauthier and Giulia Baracchini and Colleen Hughes and Patrick Hewan and Jennifer Tremblay-Mercier and Pedro Rosa-Neto and Judes Poirier and Sylvia Villeneuve and Taylor W Schmitz and Gary R Turner and R Nathan Spreng and },

doi = {10.1038/s41467-024-48490-z},

issn = {2041-1723},

year  = {2024},

date = {2024-06-01},

journal = {Nat Commun},

volume = {15},

number = {1},

pages = {4706},

abstract = {The neuromodulatory subcortical nuclei within the isodendritic core (IdC) are the earliest sites of tauopathy in Alzheimer's disease (AD). They project broadly throughout the brain's white matter. We investigated the relationship between IdC microstructure and whole-brain white matter microstructure to better understand early neuropathological changes in AD. Using multiparametric quantitative magnetic resonance imaging we observed two covariance patterns between IdC and white matter microstructure in 133 cognitively unimpaired older adults (age 67.9 ± 5.3 years) with familial risk for AD. IdC integrity related to 1) whole-brain neurite density, and 2) neurite orientation dispersion in white matter tracts known to be affected early in AD. Pattern 2 was associated with CSF concentration of phosphorylated-tau, indicating AD specificity. Apolipoprotein-E4 carriers expressed both patterns more strongly than non-carriers. IdC microstructure variation is reflected in white matter, particularly in AD-affected tracts, highlighting an early mechanism of pathological development.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38253819,

title = {The influence of APOE status on rate of cognitive decline},

author = {Cassandra Morrison and Michael D Oliver and Virginia Berry and Farooq Kamal and Mahsa Dadar},

doi = {10.1007/s11357-024-01069-4},

issn = {2509-2723},

year  = {2024},

date = {2024-06-01},

journal = {Geroscience},

volume = {46},

number = {3},

pages = {3263--3274},

abstract = {BACKGROUND: Apolipoprotein (APOE) ɛ4 positivity and subjective cognitive decline (SCD) both increase risk of Alzheimer's disease (AD) development. However, few studies have examined the relationship between SCD and APOE status, especially using longitudinal data. The current study examined whether APOE is associated with the rate of cognitive change in SCD and mild cognitive impairment (MCI).nnMETHODS: A sample of 3494 older adults (1990 normal controls, NC, 775 SCD, and 729 MCI) with a mean follow-up of 9.09 years were included from the Rush Alzheimer's Disease Center Research Sharing Hub. Linear mixed effects models examined the relationship between APOE status and cognitive change in older adults with SCD normal controls, and people with MCI.nnRESULTS: The presence of at least one ɛ2 allele in SCD and MCI results in cognitive change rates similar to a NC with the ɛ3ɛ3 genotype. Older adult SCD-ɛ4 individuals exhibited increased rate of cognitive decline compared to all groups, including NC-ɛ4 and MCI-ɛ4.nnCONCLUSION: People with SCD with at least one ɛ4 allele experience increased rates of cognitive decline compared to cognitively healthy older adults and people with MCI. These findings have important implications for treatments and interventions and can improve future research and clinical trials by targeting people in the preclinical AD phase (i.e., SCD) who also possess at least one APOE ɛ4 allele.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38817112,

title = {Circadian Regulation of Leishmania Parasite Internalisation in Macrophages and Downstream Cellular Events},

author = {Priscilla Carvalho Cabral and Sophia K Stegeman and Martin Olivier and Nicolas Cermakian},

doi = {10.1111/pim.13053},

issn = {1365-3024},

year  = {2024},

date = {2024-06-01},

journal = {Parasite Immunol},

volume = {46},

number = {6},

pages = {e13053},

abstract = {Leishmania spp. parasites use macrophages as a host cell during infection. As a result, macrophages have a dual role: clearing the parasite as well as acting as host cells. Recently, studies have shown that macrophages harbour circadian clocks, which affect many of their functions such as phagocytosis, receptor expression and cytokine release. Interestingly, Leishmania major infection in hosts was also shown to be under circadian control. Therefore, we decided to investigate what underlies the rhythms of L. major infection within macrophages. Using a culture model of infection of bone marrow-derived macrophages with L. major promastigotes, we show that the parasites are internalised into macrophages with a 24-h variation dependent on a functional circadian clock in the cells. This was associated with a variation in the number of parasites per macrophage. The cell surface expression of parasite receptors was not controlled by the cells' circadian clock. In contrast, the expression of the components of the endocytic pathway, EEA1 and LC3b, varied according to the time of infection. This was paralleled by variations in parasite-induced ROS production as well as cytokine tumour necrosis factor α. In summary, we have uncovered a time-dependent regulation of the internalisation of L. major promastigotes in macrophages, controlled by the circadian clock in these cells, as well as subsequent cellular events in the endocytic pathway, intracellular signalling and cytokine production.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38761439,

title = {Faster pace of hippocampal growth mediates the association between perinatal adversity and childhood depression},

author = {Jonas G Miller and Peter D Gluckman and Marielle V Fortier and Yap Seng Chong and Michael J Meaney and Ai Peng Tan and Ian H Gotlib},

doi = {10.1016/j.dcn.2024.101392},

issn = {1878-9307},

year  = {2024},

date = {2024-06-01},

journal = {Dev Cogn Neurosci},

volume = {67},

pages = {101392},

abstract = {Early life adversity has been posited to influence the pace of structural neurodevelopment. Most research, however, has relied on cross-sectional data, which do not reveal whether the pace of neurodevelopmental change is accelerated or slowed following early exposures. In a birth cohort study that included neuroimaging data obtained at 4.5, 6, and 7.5 years of age (N = 784), we examined associations among a cumulative measure of perinatal adversity relative to resources, nonlinear trajectories of hippocampal and amygdala volume, and children's subsequent depressive symptoms at 8.5 years of age. Greater adversity was associated with reduced bilateral hippocampal body volume in early childhood, but also to faster growth in the right hippocampal body across childhood. Further, the association between adversity and childhood depressive symptoms was mediated by faster hippocampal body growth. These findings suggest that perinatal adversity is biologically embedded in hippocampal structure development, including an accelerated pace of change in the right hippocampal body that is implicated in children's psychopathology risk. In addition, our findings suggest that reduced hippocampal volume is not inconsistent with accelerated hippocampal change; these aspects of structural development may typically co-occur, as smaller regional volumes in early childhood were associated with faster growth across childhood.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38757600,

title = {The environment and the internal clocks: The study of their relationships from prehistoric to modern times},

author = {Yvan Touitou and Nicolas Cermakian and Catherine Touitou},

doi = {10.1080/07420528.2024.2353857},

issn = {1525-6073},

year  = {2024},

date = {2024-06-01},

journal = {Chronobiol Int},

volume = {41},

number = {6},

pages = {859--887},

abstract = {The origin of biological rhythms goes back to the very beginning of life. They are observed in the animal and plant world at all levels of organization, from cells to ecosystems. As early as the 18th century, plant scientists were the first to explain the relationship between flowering cycles and environmental cycles, emphasizing the importance of daily light-dark cycles and the seasons. Our temporal structure is controlled by external and internal rhythmic signals. Light is the main synchronizer of the circadian system, as daily exposure to light entrains our clock over 24 hours, the endogenous period of the circadian system being close to, but not exactly, 24 hours. In 1960, a seminal scientific meeting, the Cold Spring Harbor Symposium on Biological Rhythms, brought together all the biological rhythms scientists of the time, a number of whom are considered the founders of modern chronobiology. All aspects of biological rhythms were addressed, from the properties of circadian rhythms to their practical and ecological aspects. Birth of chronobiology dates from this period, with the definition of its vocabulary and specificities in metabolism, photoperiodism, animal physiology, etc. At around the same time, and right up to the present day, research has focused on melatonin, the circadian neurohormone of the pineal gland, with data on its pattern, metabolism, control by light and clinical applications. However, light has a double face, as it has positive effects as a circadian clock entraining agent, but also deleterious effects, as it can lead to chronodisruption when exposed chronically at night, which can increase the risk of cancer and other diseases. Finally, research over the past few decades has unraveled the anatomical location of circadian clocks and their cellular and molecular mechanisms. This recent research has in turn allowed us to explain how circadian rhythms control physiology and health.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38739983,

title = {Model of perinatal care but not prenatal stress exposure is associated with birthweight and gestational age at Birth: The Australian birth in the time of COVID (BITTOC) study},

author = {Mia A McLean and Chloé Klimos and Belinda Lequertier and Hazel Keedle and Guillaume Elgbeili and Sue Kildea and Suzanne King and Hannah G Dahlen},

doi = {10.1016/j.srhc.2024.100981},

issn = {1877-5764},

year  = {2024},

date = {2024-06-01},

journal = {Sex Reprod Healthc},

volume = {40},

pages = {100981},

abstract = {OBJECTIVE: The present study aimed to understand, relative to standard care, whether continuity of care models (private midwifery, continuity of care with a private doctor, continuity of care with a public midwife), and women's experience of maternity care provision, during the perinatal period buffered the association between prenatal maternal stress (PNMS) and infant birth outcomes (gestational age [GA], birth weight [BW] and birth weight for gestational age [BW for GA]).nnMETHODS: 2207 women who were pregnant in Australia while COVID-19 restrictions were in place reported on their COVID-19 related objective hardship and subjective distress during pregnancy and provided information on their model of maternity care. Infant birth outcomes (BW, GA) were reported on at 2-months postpartum.nnRESULTS: Multiple linear regressions showed no relationship between PNMS and infant BW, GA or BW for GA, and neither experienced continuity of care, nor model of maternity care moderated this relationship. However, compared with all other models of care, women enrolled in private midwifery care reported the highest levels of experienced continuity of care and birthed infants at higher GA. BW and BW for GA were higher in private midwifery care, relative to standard care.nnCONCLUSION: Enrollment in continuous models of perinatal care may be a better predictor of infant birth outcomes than degree of PNMS exposure. These results highlight the possibility that increased, continuous support to women during pregnancy may play an important role in ensuring positive infant birth outcomes during future pandemics.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38526098b,

title = {Longer sleep duration and neuroinflammation in at-risk elderly with a parental history of Alzheimer's disease},

author = {Andrée-Ann Baril and Cynthia Picard and Anne Labonté and Erlan Sanchez and Catherine Duclos and Béry Mohammediyan and John C S Breitner and Sylvia Villeneuve and Judes Poirier and },

doi = {10.1093/sleep/zsae081},

issn = {1550-9109},

year  = {2024},

date = {2024-06-01},

journal = {Sleep},

volume = {47},

number = {6},

abstract = {STUDY OBJECTIVES: Although short sleep could promote neurodegeneration, long sleep may be a marker of ongoing neurodegeneration, potentially as a result of neuroinflammation. The objective was to evaluate sleep patterns with age of expected Alzheimer's disease (AD) onset and neuroinflammation.nnMETHODS: We tested 203 dementia-free participants (68.5 ± 5.4 years old, 78M). The PREVENT-AD cohort includes older persons with a parental history of AD whose age was nearing their expected AD onset. We estimated expected years to AD onset by subtracting the participants' age from their parent's at AD dementia onset. We extracted actigraphy sleep variables of interest (times of sleep onset and morning awakening, time in bed, sleep efficiency, and sleep duration) and general profiles (sleep fragmentation, phase delay, and hypersomnia). Cerebrospinal fluid (CSF) inflammatory biomarkers were assessed with OLINK multiplex technology.nnRESULTS: Proximity to, or exceeding, expected age of onset was associated with a sleep profile suggestive of hypersomnia (longer sleep and later morning awakening time). This hypersomnia sleep profile was associated with higher CSF neuroinflammatory biomarkers (IL-6, MCP-1, and global score). Interaction analyses revealed that some of these sleep-neuroinflammation associations were present mostly in those closer/exceeding the age of expected AD onset, APOE4 carriers, and those with better memory performance.nnCONCLUSIONS: Proximity to, or exceeding, parental AD dementia onset was associated with a longer sleep pattern, which was related to elevated proinflammatory CSF biomarkers. We speculate that longer sleep may serve a compensatory purpose potentially triggered by neuroinflammation as individuals are approaching AD onset. Further studies should investigate whether neuroinflammatory-triggered long sleep duration could mitigate cognitive deficits.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38623965,

title = {Neurobehavioral Mechanisms Influencing the Association Between Generativity, the Desire to Promote Well-Being of Younger Generations, and Purpose in Life in Older Adults at Risk for Alzheimer's Disease},

author = {Caitlin S Walker and Linda Li and Giulia Baracchini and Jennifer Tremblay-Mercier and R Nathan Spreng and  and Maiya R Geddes},

doi = {10.1093/geronb/gbae060},

issn = {1758-5368},

year  = {2024},

date = {2024-06-01},

journal = {J Gerontol B Psychol Sci Soc Sci},

volume = {79},

number = {6},

abstract = {OBJECTIVES: Generativity, the desire and action to improve the well-being of younger generations, is associated with purpose in life among older adults. However, the neurobehavioral factors supporting the relationship between generativity and purpose in life remain unknown. This study aims to identify the functional neuroanatomy of generativity and mechanisms linking generativity with purpose in life in at-risk older adults.nnMETHODS: Fifty-eight older adults (mean age = 70.8, SD = 5.03, 45 females) with a family history of Alzheimer's disease (AD) were recruited from the PREVENT-AD cohort. Participants underwent brain imaging and completed questionnaires assessing generativity, social support, and purpose in life. Mediation models examined whether social support mediated the association between generativity and purpose in life. Seed-to-voxel analyses investigated the association between generativity and resting-state functional connectivity (rsFC) to the ventromedial prefrontal cortex (vmPFC) and ventral striatum (VS), and whether this rsFC moderated the relationship between generativity and purpose in life.nnRESULTS: Affectionate social support mediated the association between generative desire and purpose in life. Generative desire was associated with rsFC between VS and precuneus, and, vmPFC and right dorsolateral prefrontal cortex (rdlPFC). The vmPFC-rdlPFC rsFC moderated the association between generative desire and purpose in life.nnDISCUSSION: These findings provide insight into how the brain supports complex social behavior and, separately, purpose in life in at-risk aging. Affectionate social support may be a putative target process to enhance purpose in life in older adults. This knowledge contributes to future developments of personalized interventions that promote healthy aging.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38678736,

title = {Neuromelanin levels in individuals with substance use disorders: A systematic review and meta-analysis},

author = {Jessica Ahrens and Farida Zaher and Rachel A Rabin and Clifford M Cassidy and Lena Palaniyappan},

doi = {10.1016/j.neubiorev.2024.105690},

issn = {1873-7528},

year  = {2024},

date = {2024-06-01},

journal = {Neurosci Biobehav Rev},

volume = {161},

pages = {105690},

abstract = {Dopamine's role in addiction has been extensively studied, revealing disruptions in its functioning throughout all addiction stages. Neuromelanin in the substantia nigra (SN) may reflect dopamine auto-oxidation, and can be quantified using neuromelaninsensitive magnetic resonance imaging (neuromelanin-MRI) in a non-invasive manner.In this pre-registered systematic review, we assess the current body of evidence related to neuromelanin levels in substance use disorders, using both post-mortem and MRI examinations. The systematic search identified 10 relevant articles, primarily focusing on the substantia nigra. An early-stage meta-analysis (n = 6) revealed varied observations ranging from standardized mean differences of -3.55 to +0.62, with a pooled estimate of -0.44 (95 % CI = -1.52, 0.65), but there was insufficient power to detect differences in neuromelanin content among individuals with substance use disorders. Our gap analysis highlights the lack of sufficient replication studies, with existing studies lacking the power to detect a true difference, and a complete lack of neuromelanin studies on certain substances of clinical interest. We provide recommendations for future studies of dopaminergic neurobiology in addictions and related psychiatric comorbidities.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38908100,

title = {The neurophysiological brain-fingerprint of Parkinson's disease},

author = {Jason da Silva Castanheira and Alex I Wiesman and Justine Y Hansen and Bratislav Misic and Sylvain Baillet and  and },

doi = {10.1016/j.ebiom.2024.105201},

issn = {2352-3964},

year  = {2024},

date = {2024-06-01},

journal = {EBioMedicine},

volume = {105},

pages = {105201},

abstract = {BACKGROUND: Research in healthy young adults shows that characteristic patterns of brain activity define individual "brain-fingerprints" that are unique to each person. However, variability in these brain-fingerprints increases in individuals with neurological conditions, challenging the clinical relevance and potential impact of the approach. Our study shows that brain-fingerprints derived from neurophysiological brain activity are associated with pathophysiological and clinical traits of individual patients with Parkinson's disease (PD).nnMETHODS: We created brain-fingerprints from task-free brain activity recorded through magnetoencephalography in 79 PD patients and compared them with those from two independent samples of age-matched healthy controls (N = 424 total). We decomposed brain activity into arrhythmic and rhythmic components, defining distinct brain-fingerprints for each type from recording durations of up to 4 min and as short as 30 s.nnFINDINGS: The arrhythmic spectral components of cortical activity in patients with Parkinson's disease are more variable over short periods, challenging the definition of a reliable brain-fingerprint. However, by isolating the rhythmic components of cortical activity, we derived brain-fingerprints that distinguished between patients and healthy controls with about 90% accuracy. The most prominent cortical features of the resulting Parkinson's brain-fingerprint are mapped to polyrhythmic activity in unimodal sensorimotor regions. Leveraging these features, we also demonstrate that Parkinson's symptom laterality can be decoded directly from cortical neurophysiological activity. Furthermore, our study reveals that the cortical topography of the Parkinson's brain-fingerprint aligns with that of neurotransmitter systems affected by the disease's pathophysiology.nnINTERPRETATION: The increased moment-to-moment variability of arrhythmic brain-fingerprints challenges patient differentiation and explains previously published results. We outline patient-specific rhythmic brain signaling features that provide insights into both the neurophysiological signature and symptom laterality of Parkinson's disease. Thus, the proposed definition of a rhythmic brain-fingerprint of Parkinson's disease may contribute to novel, refined approaches to patient stratification. Symmetrically, we discuss how rhythmic brain-fingerprints may contribute to the improved identification and testing of therapeutic neurostimulation targets.nnFUNDING: Data collection and sharing for this project was provided by the Quebec Parkinson Network (QPN), the Pre-symptomatic Evaluation of Novel or Experimental Treatments for Alzheimer's Disease (PREVENT-AD; release 6.0) program, the Cambridge Centre for Aging Neuroscience (Cam-CAN), and the Open MEG Archives (OMEGA). The QPN is funded by a grant from Fonds de Recherche du Québec - Santé (FRQS). PREVENT-AD was launched in 2011 as a $13.5 million, 7-year public-private partnership using funds provided by McGill University, the FRQS, an unrestricted research grant from Pfizer Canada, the Levesque Foundation, the Douglas Hospital Research Centre and Foundation, the Government of Canada, and the Canada Fund for Innovation. The Brainstorm project is supported by funding to SB from the NIH (R01-EB026299-05). Further funding to SB for this study included a Discovery grant from the Natural Sciences and Engineering Research Council of Canada of Canada (436355-13), and the CIHR Canada research Chair in Neural Dynamics of Brain Systems (CRC-2017-00311).},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38919577,

title = {Development and validation of home-based psychosocial self-management interventions in schizophrenia and related disorders in low-resource settings: A mixed methods approach},

author = {Rakesh K Chadda and Mamta Sood and Nishtha Chawla and Ananya Mahapatra and Rekha Patel and MohaPradeep Mohan and Srividya N Iyer and Padmavati Ramachandran and Thara Rangaswamy and Jai Shah and Jason Madan and Max Birchwood and Caroline Meyer and Richard Lilford and Vivek Furtado and Currie Graeme and Swaran P Singh},

doi = {10.4103/indianjpsychiatry.indianjpsychiatry_610_23},

issn = {0019-5545},

year  = {2024},

date = {2024-05-01},

journal = {Indian J Psychiatry},

volume = {66},

number = {5},

pages = {440--448},

abstract = {BACKGROUND: Psychosocial interventions, crucial for recovery in patients with schizophrenia, have often been developed and tested in high income countries. We aimed at developing and validating home-based a booklet based psycho-social intervention with inputs from stakeholders: patients, families, and mental health professionals (MHP) for patients with schizophrenia and related disorders in low resource settings.nnMETHODS: We developed a preliminary version of psychosocial intervention booklets based on six themes derived from focus group discussions conducted with patients, families, and MHP. Initially, quantitative assessment of content validity was done by MHP on overall and Content Validity Index of individual items of the specific booklets, followed by in-depth interviews about their views. The booklets were modified based on their inputs. Further, pilot testing of manuals was done on the users - nine pairs of patients and caregivers followed by development of a final version of psycho-social intervention.nnRESULTS: The percentage content validity of individual modules and overall booklets was ≥78.5% indicating good validity. Most MHP reported that the manuals were relevant and easy to use but were text-heavy, and lengthy. On pilot testing of modified manuals with patients and their family caregivers, majority (77.8%) of them found booklets useful and suggested that there should be separate booklets for both patients and caregivers for providing information and entering separate response for the activities, integrating helpful tips. Language should be simple. Finally, two sets of booklets ("info book" and "workbook") named 'Saksham' (meaning empowered) were created with specific modules (viz., 'Medicine adherence', 'Daily routine', 'Eating right', 'Physical activity', 'Physical health monitoring', 'Self-reliance', and 'Psychoeducation') for patients and caregivers each, in two languages (Hindi and English).nnCONCLUSION: Booklets with modules for psychosocial interventions for patients with schizophrenia and their caregivers were developed after establishing content validity and pilot testing.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid37992295,

title = {Insulin-like growth factor binding protein-2 in at-risk adults and autopsy-confirmed Alzheimer brains},

author = {Marc James Quesnel and Anne Labonté and Cynthia Picard and Henrik Zetterberg and Kaj Blennow and Ann Brinkmalm and Sylvia Villeneuve and Judes Poirier and  and },

doi = {10.1093/brain/awad398},

issn = {1460-2156},

year  = {2024},

date = {2024-05-01},

journal = {Brain},

volume = {147},

number = {5},

pages = {1680--1695},

abstract = {Insulin, insulin-like growth factors (IGF) and their receptors are highly expressed in the adult hippocampus. Thus, disturbances in the insulin-IGF signalling pathway may account for the selective vulnerability of the hippocampus to nascent Alzheimer's disease (AD) pathology. In the present study, we examined the predominant IGF-binding protein in the CSF, IGFBP2. CSF was collected from 109 asymptomatic members of the parental history-positive PREVENT-AD cohort. CSF levels of IGFBP2, core AD and synaptic biomarkers were measured using proximity extension assay, ELISA and mass spectrometry. Cortical amyloid-beta (Aβ) and tau deposition were examined using 18F-NAV4694 and flortaucipir. Cognitive assessments were performed during up to 8 years of follow-up, using the Repeatable Battery for the Assessment of Neuropsychological Status. T1-weighted structural MRI scans were acquired, and neuroimaging analyses were performed on pre-specified temporal and parietal brain regions. Next, in an independent cohort, we allocated 241 dementia-free ADNI-1 participants into four stages of AD progression based on the biomarkers CSF Aβ42 and total-tau (t-tau). In this analysis, differences in CSF and plasma IGFBP2 levels were examined across the pathological stages. Finally, IGFBP2 mRNA and protein levels were examined in the frontal cortex of 55 autopsy-confirmed AD and 31 control brains from the Quebec Founder Population (QFP) cohort, a unique population isolated from Eastern Canada. CSF IGFBP2 progressively increased over 5 years in asymptomatic PREVENT-AD participants. Baseline CSF IGFBP2 was positively correlated with CSF AD biomarkers and synaptic biomarkers, and negatively correlated with longitudinal changes in delayed memory (P = 0.024) and visuospatial abilities (P = 0.019). CSF IGFBP2 was negatively correlated at a trend-level with entorhinal cortex volume (P = 0.082) and cortical thickness in the piriform (P = 0.039), inferior temporal (P = 0.008), middle temporal (P = 0.014) and precuneus (P = 0.033) regions. In ADNI-1, CSF (P = 0.009) and plasma (P = 0.001) IGFBP2 were significantly elevated in Stage 2 [CSF Aβ(+)/t-tau(+)]. In survival analyses in ADNI-1, elevated plasma IGFBP2 was associated with a greater rate of AD conversion (hazard ratio = 1.62, P = 0.021). In the QFP cohort, IGFBP2 mRNA was reduced (P = 0.049); however, IGFBP2 protein levels did not differ in the frontal cortex of autopsy-confirmed AD brains (P = 0.462). Nascent AD pathology may induce an upregulation in IGFBP2 in asymptomatic individuals. CSF and plasma IGFBP2 may be valuable markers for identifying CSF Aβ(+)/t-tau(+) individuals and those with a greater risk of AD conversion.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38441248,

title = {A systematic review of altered resting-state networks in early deafness and implications for cochlear implantation outcomes},

author = {Zahra Jafari and Bryan E Kolb and Majid H Mohajerani},

doi = {10.1111/ejn.16295},

issn = {1460-9568},

year  = {2024},

date = {2024-05-01},

journal = {Eur J Neurosci},

volume = {59},

number = {10},

pages = {2596--2615},

abstract = {Auditory deprivation following congenital/pre-lingual deafness (C/PD) can drastically affect brain development and its functional organisation. This systematic review intends to extend current knowledge of the impact of C/PD and deafness duration on brain resting-state networks (RSNs), review changes in RSNs and spoken language outcomes post-cochlear implant (CI) and draw conclusions for future research. The systematic literature search followed the PRISMA guideline. Two independent reviewers searched four electronic databases using combined keywords: 'auditory deprivation', 'congenital/prelingual deafness', 'resting-state functional connectivity' (RSFC), 'resting-state fMRI' and 'cochlear implant'. Seventeen studies (16 cross-sectional and one longitudinal) met the inclusion criteria. Using the Crowe Critical Appraisal Tool, the publications' quality was rated between 65.0% and 92.5% (mean: 84.10%), ≥80% in 13 out of 17 studies. A few studies were deficient in sampling and/or ethical considerations. According to the findings, early auditory deprivation results in enhanced RSFC between the auditory network and brain networks involved in non-verbal communication, and high levels of spontaneous neural activity in the auditory cortex before CI are evidence of occupied auditory cortical areas with other sensory modalities (cross-modal plasticity) and sub-optimal CI outcomes. Overall, current evidence supports the idea that moreover intramodal and cross-modal plasticity, the entire brain adaptation following auditory deprivation contributes to spoken language development and compensatory behaviours.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38623902,

title = {Longitudinal cerebral perfusion in presymptomatic genetic frontotemporal dementia: GENFI results.},

author = {Maurice Pasternak and Saira S Mirza and Nicholas Luciw and Henri J M M Mutsaerts and Jan Petr and David Thomas and David Cash and Martina Bocchetta and Maria Carmela Tartaglia and Sara B Mitchell and Sandra E Black and Morris Freedman and David Tang-Wai and Ekaterina Rogaeva and Lucy L Russell and Arabella Bouzigues and John C van Swieten and Lize C Jiskoot and Harro Seelaar and Robert Laforce and Pietro Tiraboschi and Barbara Borroni and Daniela Galimberti and James B Rowe and Caroline Graff and Elizabeth Finger and Sandro Sorbi and Alexandre de Mendonça and Chris Butler and Alex Gerhard and Raquel Sanchez-Valle and Fermin Moreno and Matthis Synofzik and Rik Vandenberghe and Simon Ducharme and Johannes Levin and Markus Otto and Isabel Santana and Antonio P Strafella and Bradley J MacIntosh and Jonathan D Rohrer and Mario Masellis and GENetic Frontotemporal dementia Initiative (GENFI).},

doi = {10.1002/alz.13750},

issn = {1552-5279},

year  = {2024},

date = {2024-05-01},

urldate = {2024-05-01},

journal = {Alzheimers Dement},

volume = {20},

number = {5},

pages = {3525--3542},

abstract = {INTRODUCTION: Effective longitudinal biomarkers that track disease progression are needed to characterize the presymptomatic phase of genetic frontotemporal dementia (FTD). We investigate the utility of cerebral perfusion as one such biomarker in presymptomatic FTD mutation carriers.nnMETHODS: We investigated longitudinal profiles of cerebral perfusion using arterial spin labeling magnetic resonance imaging in 42 C9orf72, 70 GRN, and 31 MAPT presymptomatic carriers and 158 non-carrier controls. Linear mixed effects models assessed perfusion up to 5 years after baseline assessment.nnRESULTS: Perfusion decline was evident in all three presymptomatic groups in global gray matter. Each group also featured its own regional pattern of hypoperfusion over time, with the left thalamus common to all groups. Frontal lobe regions featured lower perfusion in those who symptomatically converted versus asymptomatic carriers past their expected age of disease onset.nnDISCUSSION: Cerebral perfusion is a potential biomarker for assessing genetic FTD and its genetic subgroups prior to symptom onset.nnHIGHLIGHTS: Gray matter perfusion declines in at-risk genetic frontotemporal dementia (FTD). Regional perfusion decline differs between at-risk genetic FTD subgroups . Hypoperfusion in the left thalamus is common across all presymptomatic groups. Converters exhibit greater right frontal hypoperfusion than non-converters past their expected conversion date. Cerebral hypoperfusion is a potential early biomarker of genetic FTD.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38631765,

title = {MAPT H2 haplotype and risk of Pick's disease in the Pick's disease International Consortium: a genetic association study},

author = {Rebecca R Valentino and William J Scotton and Shanu F Roemer and Tammaryn Lashley and Michael G Heckman and Maryam Shoai and Alejandro Martinez-Carrasco and Nicole Tamvaka and Ronald L Walton and Matthew C Baker and Hannah L Macpherson and Raquel Real and Alexandra I Soto-Beasley and Kin Mok and Tamas Revesz and Elizabeth A Christopher and Michael DeTure and William W Seeley and Edward B Lee and Matthew P Frosch and Laura Molina-Porcel and Tamar Gefen and Javier Redding-Ochoa and Bernardino Ghetti and Andrew C Robinson and Christopher Kobylecki and James B Rowe and Thomas G Beach and Andrew F Teich and Julia L Keith and Istvan Bodi and Glenda M Halliday and Marla Gearing and Thomas Arzberger and Christopher M Morris and Charles L White and Naguib Mechawar and Susana Boluda and Ian R MacKenzie and Catriona McLean and Matthew D Cykowski and Shih-Hsiu J Wang and Caroline Graff and Rashed M Nagra and Gabor G Kovacs and Giorgio Giaccone and Manuela Neumann and Lee-Cyn Ang and Agostinho Carvalho and Huw R Morris and Rosa Rademakers and John A Hardy and Dennis W Dickson and Jonathan D Rohrer and Owen A Ross and },

doi = {10.1016/S1474-4422(24)00083-8},

issn = {1474-4465},

year  = {2024},

date = {2024-05-01},

journal = {Lancet Neurol},

volume = {23},

number = {5},

pages = {487--499},

abstract = {BACKGROUND: Pick's disease is a rare and predominantly sporadic form of frontotemporal dementia that is classified as a primary tauopathy. Pick's disease is pathologically defined by the presence in the frontal and temporal lobes of Pick bodies, composed of hyperphosphorylated, three-repeat tau protein, encoded by the MAPT gene. MAPT has two distinct haplotypes, H1 and H2; the MAPT H1 haplotype is the major genetic risk factor for four-repeat tauopathies (eg, progressive supranuclear palsy and corticobasal degeneration), and the MAPT H2 haplotype is protective for these disorders. The primary aim of this study was to evaluate the association of MAPT H2 with Pick's disease risk, age at onset, and disease duration.nnMETHODS: In this genetic association study, we used data from the Pick's disease International Consortium, which we established to enable collection of data from individuals with pathologically confirmed Pick's disease worldwide. For this analysis, we collected brain samples from individuals with pathologically confirmed Pick's disease from 35 sites (brainbanks and hospitals) in North America, Europe, and Australia between Jan 1, 2020, and Jan 31, 2023. Neurologically healthy controls were recruited from the Mayo Clinic (FL, USA, or MN, USA between March 1, 1998, and Sept 1, 2019). For the primary analysis, individuals were directly genotyped for the MAPT H1-H2 haplotype-defining variant rs8070723. In a secondary analysis, we genotyped and constructed the six-variant-defined (rs1467967-rs242557-rs3785883-rs2471738-rs8070723-rs7521) MAPT H1 subhaplotypes. Associations of MAPT variants and MAPT haplotypes with Pick's disease risk, age at onset, and disease duration were examined using logistic and linear regression models; odds ratios (ORs) and β coefficients were estimated and correspond to each additional minor allele or each additional copy of the given haplotype.nnFINDINGS: We obtained brain samples from 338 people with pathologically confirmed Pick's disease (205 [61%] male and 133 [39%] female; 338 [100%] White) and 1312 neurologically healthy controls (611 [47%] male and 701 [53%] female; 1312 [100%] White). The MAPT H2 haplotype was associated with increased risk of Pick's disease compared with the H1 haplotype (OR 1·35 [95% CI 1·12 to 1·64], p=0·0021). MAPT H2 was not associated with age at onset (β -0·54 [95% CI -1·94 to 0·87], p=0·45) or disease duration (β 0·05 [-0·06 to 0·16], p=0·35). Although not significant after correcting for multiple testing, associations were observed at p less than 0·05: with risk of Pick's disease for the H1f subhaplotype (OR 0·11 [0·01 to 0·99], p=0·049); with age at onset for H1b (β 2·66 [0·63 to 4·70], p=0·011), H1i (β -3·66 [-6·83 to -0·48], p=0·025), and H1u (β -5·25 [-10·42 to -0·07], p=0·048); and with disease duration for H1x (β -0·57 [-1·07 to -0·07], p=0·026).nnINTERPRETATION: The Pick's disease International Consortium provides an opportunity to do large studies to enhance our understanding of the pathobiology of Pick's disease. This study shows that, in contrast to the decreased risk of four-repeat tauopathies, the MAPT H2 haplotype is associated with an increased risk of Pick's disease in people of European ancestry. This finding could inform development of isoform-related therapeutics for tauopathies.nnFUNDING: Wellcome Trust, Rotha Abraham Trust, Brain Research UK, the Dolby Fund, Dementia Research Institute (Medical Research Council), US National Institutes of Health, and the Mayo Clinic Foundation.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38704445,

title = {Personalized whole-brain neural mass models reveal combined Aβ and tau hyperexcitable influences in Alzheimer's disease},

author = {Lazaro M Sanchez-Rodriguez and Gleb Bezgin and Felix Carbonell and Joseph Therriault and Jaime Fernandez-Arias and Stijn Servaes and Nesrine Rahmouni and Cécile Tissot and Jenna Stevenson and Thomas K Karikari and Nicholas J Ashton and Andréa L Benedet and Henrik Zetterberg and Kaj Blennow and Gallen Triana-Baltzer and Hartmuth C Kolb and Pedro Rosa-Neto and Yasser Iturria-Medina},

doi = {10.1038/s42003-024-06217-2},

issn = {2399-3642},

year  = {2024},

date = {2024-05-01},

journal = {Commun Biol},

volume = {7},

number = {1},

pages = {528},

abstract = {Neuronal dysfunction and cognitive deterioration in Alzheimer's disease (AD) are likely caused by multiple pathophysiological factors. However, mechanistic evidence in humans remains scarce, requiring improved non-invasive techniques and integrative models. We introduce personalized AD computational models built on whole-brain Wilson-Cowan oscillators and incorporating resting-state functional MRI, amyloid-β (Aβ) and tau-PET from 132 individuals in the AD spectrum to evaluate the direct impact of toxic protein deposition on neuronal activity. This subject-specific approach uncovers key patho-mechanistic interactions, including synergistic Aβ and tau effects on cognitive impairment and neuronal excitability increases with disease progression. The data-derived neuronal excitability values strongly predict clinically relevant AD plasma biomarker concentrations (p-tau217, p-tau231, p-tau181, GFAP) and grey matter atrophy obtained through voxel-based morphometry. Furthermore, reconstructed EEG proxy quantities show the hallmark AD electrophysiological alterations (theta band activity enhancement and alpha reductions) which occur with Aβ-positivity and after limbic tau involvement. Microglial activation influences on neuronal activity are less definitive, potentially due to neuroimaging limitations in mapping neuroprotective vs detrimental activation phenotypes. Mechanistic brain activity models can further clarify intricate neurodegenerative processes and accelerate preventive/treatment interventions.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38415764,

title = {Access to mental health services in urban areas: examine the availability, affordability, and accessibility of mental health services in urban settings, particularly for individuals with intersecting marginalized identities},

author = {Xiangfei Meng},

doi = {10.1097/YCO.0000000000000924},

issn = {1473-6578},

year  = {2024},

date = {2024-05-01},

journal = {Curr Opin Psychiatry},

volume = {37},

number = {3},

pages = {185--190},

abstract = {PURPOSE OF REVIEW: To offer an integrative overview of mental health services in urban areas across different social groups and underscore the challenges and potential solutions to improve access to mental health services in urban areas.nnRECENT FINDINGS: The process of urbanization places a lot of toll on the current mental health services system. Challenges to both mental health and mental health services include the elevated risk of some mental and behavioral health issues, the increased demand for mental health services, and the intensification of mental health inequalities. The phenomenon of mental health inequalities is exacerbated in urban areas, with certain disadvantaged population groups more likely to report higher mental health issues and difficulties in accessing mental health services. Targeted and dedicated strategies are warranted to develop and allocate resources to address the mental health services needs among those simultaneously with multiple disadvantaged social and economic characteristics.nnSUMMARY: Urbanization places a substantive burden on both mental health and mental health services and creates challenges to mental health services access. Integrative and multisectoral initiatives could shed light on effectively addressing the issues of access to mental health services in urban cities.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38412907,

title = {Maternal asthma symptoms during pregnancy on child behaviour and executive function: A Bayesian phenomics approach},

author = {Syeda Fabeha Husain and Andrea Cremaschi and Noor Hidayatul Aini Suaini and Maria De Iorio and Evelyn X L Loo and Lynette P Shek and Anne E N Goh and Michael J Meaney and Elizabeth H Tham and Evelyn C Law},

doi = {10.1016/j.bbi.2024.02.028},

issn = {1090-2139},

year  = {2024},

date = {2024-05-01},

journal = {Brain Behav Immun},

volume = {118},

pages = {202--209},

abstract = {OBJECTIVE: Maternal history of inflammatory conditions has been linked to offspring developmental and behavioural outcomes. This phenomenon may be explained by the maternal immune activation (MIA) hypothesis, which posits that dysregulation of the gestational immune environment affects foetal neurodevelopment. The timing of inflammation is critical. We aimed to understand maternal asthma symptoms during pregnancy, in contrast with paternal asthma symptoms during the same period, on child behaviour problems and executive function in a population-based cohort.nnMETHODS: Data were obtained from 844 families from the Growing Up in Singapore Towards healthy Outcomes (GUSTO) birth cohort. Parent asthma symptoms during the prenatal period were reported. Asthma symptoms in children were reported longitudinally from two to five years old, while behavioural problems and executive functioning were obtained at seven years old. Parent and child measures were compared between mothers with and without prenatal asthma symptoms. Generalized linear and Bayesian phenomics models were used to determine the relation between parent or child asthma symptoms and child outcomes.nnRESULTS: Children of mothers with prenatal asthma symptoms had greater behavioural and executive problems than controls (Cohen's d: 0.43-0.75; all p < 0.05). This association remained after adjustments for emerging asthma symptoms during the preschool years and fathers' asthma symptoms during the prenatal period. After adjusting for dependence between child outcomes, the Bayesian phenomics model showed that maternal prenatal asthma symptoms were associated with child internalising symptoms and higher-order executive function, while child asthma symptoms were associated with executive function skills. Paternal asthma symptoms during the prenatal period were not associated with child outcomes.nnCONCLUSIONS: Associations between child outcomes and maternal but not paternal asthma symptoms during the prenatal period suggests a role for MIA. These findings need to be validated in larger samples, and further research may identify behavioural and cognitive profiles of children with exposure to MIA.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38856286,

title = {Spatial-Temporal Analysis of Neural Desynchronization in Sleeplike States Reveals Critical Dynamics},

author = {Davor Curic and Surjeet Singh and Mojtaba Nazari and Majid H Mohajerani and Jörn Davidsen},

doi = {10.1103/PhysRevLett.132.218403},

issn = {1079-7114},

year  = {2024},

date = {2024-05-01},

journal = {Phys Rev Lett},

volume = {132},

number = {21},

pages = {218403},

abstract = {Sleep is characterized by nonrapid eye movement sleep, originating from widespread neuronal synchrony, and rapid eye movement sleep, with neuronal desynchronization akin to waking behavior. While these were thought to be global brain states, recent research suggests otherwise. Using time-frequency analysis of mesoscopic voltage-sensitive dye recordings of mice in a urethane-anesthetized model of sleep, we find transient neural desynchronization occurring heterogeneously across the cortex within a background of synchronized neural activity, in a manner reminiscent of a critical spreading process and indicative of an "edge-of-synchronization" phase transition.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38698406,

title = {Irregular word reading as a marker of semantic decline in Alzheimer's disease: implications for premorbid intellectual ability measurement},

author = {Anna Marier and Mahsa Dadar and Florence Bouhali and Maxime Montembeault and },

doi = {10.1186/s13195-024-01438-3},

issn = {1758-9193},

year  = {2024},

date = {2024-05-01},

journal = {Alzheimers Res Ther},

volume = {16},

number = {1},

pages = {96},

abstract = {BACKGROUND: Irregular word reading has been used to estimate premorbid intelligence in Alzheimer's disease (AD) dementia. However, reading models highlight the core influence of semantic abilities on irregular word reading, which shows early decline in AD. The primary objective of this study is to ascertain whether irregular word reading serves as an indicator of cognitive and semantic decline in AD, potentially discouraging its use as a marker for premorbid intellectual abilities.nnMETHOD: Six hundred eighty-one healthy controls (HC), 104 subjective cognitive decline, 290 early and 589 late mild cognitive impairment (EMCI, LMCI) and 348 AD participants from the Alzheimer's Disease Neuroimaging Initiative were included. Irregular word reading was assessed with the American National Adult Reading Test (AmNART). Multiple linear regressions were conducted predicting AmNART score using diagnostic category, general cognitive impairment and semantic tests. A generalized logistic mixed-effects model predicted correct reading using extracted psycholinguistic characteristics of each AmNART words. Deformation-based morphometry was used to assess the relationship between AmNART scores and voxel-wise brain volumes, as well as with the volume of a region of interest placed in the left anterior temporal lobe (ATL), a region implicated in semantic memory.nnRESULTS: EMCI, LMCI and AD patients made significantly more errors in reading irregular words compared to HC, and AD patients made more errors than all other groups. Across the AD continuum, as well as within each diagnostic group, irregular word reading was significantly correlated to measures of general cognitive impairment / dementia severity. Neuropsychological tests of lexicosemantics were moderately correlated to irregular word reading whilst executive functioning and episodic memory were respectively weakly and not correlated. Age of acquisition, a primarily semantic variable, had a strong effect on irregular word reading accuracy whilst none of the phonological variables significantly contributed. Neuroimaging analyses pointed to bilateral hippocampal and left ATL volume loss as the main contributors to decreased irregular word reading performances.nnCONCLUSIONS: While the AmNART may be appropriate to measure premorbid intellectual abilities in cognitively unimpaired individuals, our results suggest that it captures current semantic decline in MCI and AD patients and may therefore underestimate premorbid intelligence. On the other hand, irregular word reading tests might be clinically useful to detect semantic impairments in individuals on the AD continuum.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}